The DOI matches its Crossref record; 341 of the 341 references it cites were found in a registry or an index; none of the 257 sources its claims cite is checked for support yet.
The Airway Epithelium: Soldier in the Fight against Respiratory Viruses
Open accessAbstract
SUMMARY: The airway epithelium acts as a frontline defense against respiratory viruses, not only as a physical barrier and through the mucociliary apparatus but also through its immunological functions. It initiates multiple innate and adaptive immune mechanisms which are crucial for efficient antiviral responses. The interaction between respiratory viruses and airway epithelial cells results in production of antiviral substances, including type I and III interferons, lactoferrin, β-defensins, and nitric oxide, and also in production of cytokines and chemokines, which recruit inflammatory cells and influence adaptive immunity. These defense mechanisms usually result in rapid virus clearance. However, respiratory viruses elaborate strategies to evade antiviral mechanisms and immune responses. They may disrupt epithelial integrity through cytotoxic effects, increasing paracellular permeability and damaging epithelial repair mechanisms. In addition, they can interfere with immune responses by blocking interferon pathways and by subverting protective inflammatory responses toward detrimental ones. Finally, by inducing overt mucus secretion and mucostasis and by paving the way for bacterial infections, they favor lung damage and further impair host antiviral mechanisms.
Overview
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Written from the paper’s full text.
TL;DR
This review argues that the airway epithelium is a central frontline defender against respiratory viruses through physical barrier, mucociliary clearance, and innate/adaptive immune functions, but that viruses subvert these defenses to cause epithelial damage, dysregulated inflammation, mucus obstruction, and secondary bacterial infection. It synthesizes mechanisms of epithelial protection and viral evasion and discusses therapeutic implications.
Key findings
- The airway epithelium defends against respiratory viruses via cell-cell junctions, the mucociliary escalator, and immune recognition through TLRs and intracellular sensors such as RIG-I/MDA5; it produces antiviral substances including type I and III interferons, lactoferrin, β-defensins, and nitric oxide, plus cytokines/chemokines that recruit innate and adaptive immune cells.
- Respiratory viruses evade these defenses by inhibiting IFN synthesis or downstream signaling (e.g., RSV NS2 targets RIG-I; RSV NS1/NS2 inhibit STAT2; influenza NS1 inhibits PKR), disrupting tight junctions and epithelial repair, shifting Th1 responses toward Th2, and inducing mucus hypersecretion and mucostasis.
- Viral respiratory tract infections are the most common illnesses worldwide; rhinoviruses are the most frequent agents, and vRTIs are linked to exacerbations of asthma, cystic fibrosis, and COPD and to later recurrent wheeze/asthma risk. The paper reports that vRTIs lead to more than 400,000 hospitalizations per year among children in the United States.
- Viruses promote secondary bacterial infection: during influenza pandemics, bacterial coinfections with *Streptococcus pneumoniae*, *Haemophilus influenzae*, and *Staphylococcus aureus* contributed importantly to mortality, and the majority of deaths during the 1918–1919 flu pandemic were due to bacterial pneumonia. Mechanisms include decreased clearance, increased paracellular permeability, and virus-induced bacterial adherence.
Methods
- Design: narrative review.
- Data or sample: published literature on airway epithelial defense and respiratory virus pathogenesis; no primary cohort, experimental sample, or statistical analysis is reported.
- Main analysis: thematic synthesis of epithelial barrier, mucociliary, innate, and adaptive immune mechanisms, viral evasion strategies, and pathways promoting bacterial infection; includes summary tables of the “wounded soldier” model and studies on bacterial adherence to human respiratory epithelial cells during viral infection.
Limitations
- The paper does not state limitations.
- Evident from the text: as a narrative review, it does not describe a systematic search strategy, inclusion criteria, or quantitative synthesis, and it relies on heterogeneous in vitro, animal, and clinical studies.
- Evident from the text: several mechanisms are explicitly described as unresolved or speculative, including whether NLRP3 directly senses viral RNA, the role of airway epithelial cell-induced inflammation in virus-specific disease severity, and whether high inflammatory mediator levels reflect dysregulated inflammation versus increased viral replication.
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Claims the paper makes
152 Not checked yet · 23 Own interpretation · 14 No basis given
None of the sources cited for this claim have been checked yet.
In the paper
“Airway mucin production is induced by many respiratory viruses, including rhinovirus and influenza virus (278, 336).”
What the sources say
- Not checked yetcites [278] Tamura, S., and T. Kurata. 2004. Defense mechanisms against influenza virus infection in the respiratory tract mucosa. Jpn. J. Infect. Dis. 57:236-247. [PubMed] [Google Scholar] source
- Not checked yetcites [336] Zhu, L., P. K. Lee, W. M. Lee, Y. Zhao, D. Yu, and Y. Chen. 2009. Rhinovirus-induced major airway mucin production involves a novel TLR3-EGFR-dependent pathway. Am. J. Respir. Cell Mol. Biol. 40:610-619. [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“They are attached to their neighbors by cell-cell junctions, including tight junctions (TJs), adherens junctions (AJs), gap junctions, and desmosomes (234).”
What the sources say
- Not checked yetcites [234] Roche, W. R., S. Montefort, J. Baker, and S. T. Holgate. 1993. Cell adhesion molecules and the bronchial epithelium. Am. Rev. Respir. Dis. 148:S79-S82. [DOI] [PubMed] [Google Scholar] source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The increased production of mucus allows for better trapping and clearance of viruses.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Airway epithelial cells rapidly recognize pathogens through pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs) and intracellular viral sensors (3) (Fig. 2).”
What the sources say
- Not checked yetcites [3] Akira, S. 2009. Pathogen recognition by innate immunity and its signaling. Proc. Jpn. Acad. Ser. B Phys. Biol. Sci. 85:143-156. [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“TLRs play a crucial role in the initiation of immune responses in the respiratory epithelium (45, 175).”
What the sources say
- Not checked yetcites [45] Diamond, G., D. Legarda, and L. K. Ryan. 2000. The innate immune response of the respiratory epithelium. Immunol. Rev. 173:27-38. [DOI] [PubMed] [Google Scholar] source
- Not checked yetcites [175] Medzhitov, R. 2001. Toll-like receptors and innate immunity. Nat. Rev. Immunol. 1:135-145. [DOI] [PubMed] [Google Scholar] source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“They hinder viral access to receptors within the epithelial basolateral membrane, which is an important interaction and entry site for several viruses (18, 19).”
What the sources say
- Not checked yetcites [18] Bergelson, J. M. 2009. Intercellular junctional proteins as receptors and barriers to virus infection and spread. Cell Host Microbe 5:517-521. [DOI] [PubMed] [Google Scholar] source
- Not checked yetcites [19] Bergelson, J. M. 2003. Virus interactions with mucosal surfaces: alternative receptors, alternative pathways. Curr. Opin. Microbiol. 6:386-391. [DOI] [PubMed] [Google Scholar] source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, respiratory viruses elaborate strategies to evade antiviral mechanisms and immune responses.”
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In addition to their physical protective role, airway epithelial cells possess important immune functions in the fight against respiratory viruses.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Airway epithelial cells regulate both innate and adaptive immunity through production of functional molecules and physical interactions with cells of the immune system.”
What the sources say
- Not checked yetcites [108] Hiemstra, P. S. 2001. Epithelial antimicrobial peptides and proteins: their role in host defence and inflammation. Paediatr. Respir. Rev. 2:306-310. [DOI] [PubMed] [Google Scholar] source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The interaction between respiratory viruses and airway epithelial cells results in production of antiviral substances, including type I and III interferons, lactoferrin, β-defensins, and nitric oxide, and also in production of cytokines and chemokines, which recruit inflammatory cells and influence adaptive immunity.”
plaindirect- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 62
- Probably not a substantial claim. 20
In the paper
“Activation of epithelial cells results in immediate host defense responses that include production of antiviral substances as well as proinflammatory cytokines which recruit and activate other mucosal innate immune cells and initiate mechanisms of adaptive immunity (108).”
What the sources say
- Not checked yetcites [108] Hiemstra, P. S. 2001. Epithelial antimicrobial peptides and proteins: their role in host defence and inflammation. Paediatr. Respir. Rev. 2:306-310. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“Besides its role in maintaining the conduit for air to and from the alveoli, the airway epithelium is central to the defense of the lung against pathogens, through the combined function of ciliated epithelial and secretory cells maintaining efficient mucociliary clearance and through a variety of other host defense mechanisms (45, 65, 144).”
What the sources say
- Not checked yetcites [45] Diamond, G., D. Legarda, and L. K. Ryan. 2000. The innate immune response of the respiratory epithelium. Immunol. Rev. 173:27-38. [DOI] [PubMed] [Google Scholar]
- Not checked yetcites [65] Fokkens, W. J., and R. A. Scheeren. 2000. Upper airway defence mechanisms. Paediatr. Respir. Rev. 1:336-341. [DOI] [PubMed] [Google Scholar]
- Not checked yetcites [144] Knight, D. A., and S. T. Holgate. 2003. The airway epithelium: structural and functional properties in health and disease. Respirology 8:432-446. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The airway epithelium acts as a frontline defense against respiratory viruses, not only as a physical barrier and through the mucociliary apparatus but also through its immunological functions.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Primary human airway epithelial cells and cell lines derived from them have been shown to express 10 TLRs (TLR1 to -10) (188, 260), and TLR expression has been documented for human biopsy tissue (101).”
What the sources say
- Not checked yetcites [188] Muir, A., G. Soong, S. Sokol, B. Reddy, M. I. Gomez, A. Van Heeckeren, and A. Prince. 2004. Toll-like receptors in normal and cystic fibrosis airway epithelial cells. Am. J. Respir. Cell Mol. Biol. 30:777-783. [DOI] [PubMed] [Google Scholar] source
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plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Finally, by inducing overt mucus secretion and mucostasis and by paving the way for bacterial infections, they favor lung damage and further impair host antiviral mechanisms.”
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“While airway defense mechanisms efficiently fight respiratory viruses most of the time, resulting in rapid clearance of the virus with minimal clinical consequences, viruses have found ways of avoiding immune responses in the airways, with the potential consequence of severe respiratory disease.”
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, they can interfere with immune responses by blocking interferon pathways and by subverting protective inflammatory responses toward detrimental ones.”
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Innate immune responses of the epithelium allow for control of viral invasion and replication, and adaptive responses allow for effective viral clearance through cells of the adaptive immune system.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“However, mucin overproduction and excessive mucus formation can lead to airway obstruction and exacerbation of preexisting airway disease, turning a powerful innate cleaning defense system into a detrimental mechanism (see The Wounded Soldier) (239, 298).”
What the sources say
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“These defense mechanisms usually result in rapid virus clearance.”
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“They may disrupt epithelial integrity through cytotoxic effects, increasing paracellular permeability and damaging epithelial repair mechanisms.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Type III IFNs possess antiviral properties similar to those of type I IFNs but appear to be expressed especially by epithelial cells and consequently exert host protection primarily at epithelial surfaces (8, 9, 335).”
What the sources say
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hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Binding of RNA species to RIG-I and MDA5 leads to interaction of CARDs within an adaptor protein called IPS-1, MAVS, VISA, or Cardif (222). This outer mitochondrial membrane protein mediates the recruitment and activation of protein kinases that phosphorylate the transcription factor IRF-3, leading to the synthesis of type I and type III IFNs (155).”
What the sources say
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“For example, RSV induces replication-mediated activation of the IFN-β promoter via RIG-I signaling (253).”
What the sources say
- Not checked yetcites [253] Sasai, M., M. Shingai, K. Funami, M. Yoneyama, T. Fujita, M. Matsumoto, and T. Seya. 2006. NAK-associated protein 1 participates in both the TLR3 and the cytoplasmic pathways in type I IFN induction. J. Immunol. 177:8676-8683. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“It has been shown that the RSV fusion protein interacts with TLR4, which then signals through MyD88 to induce immune responses in airway epithelial cells (28, 92, 103, 152), and a recent study demonstrated RSV interaction with TLR2 and TLR6, promoting a proinflammatory response (190).”
What the sources say
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Among them, IFNs, lactoferrin (LF), β-defensins (BDs), and nitric oxide (NO) are considered the most important epithelium-derived antiviral host defense molecules (Fig. 1).”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“TLRs trigger activation predominantly of mitogen-activated protein (MAP) kinases and of several key transcription factors, including NF-κB, interferon regulatory factor 3 (IRF-3), and IRF-7, resulting in the induction of numerous proinflammatory cytokines and type I (α and β) and type III (λ) IFNs (120).”
What the sources say
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast, RIG-I has been shown to detect negative-sense ssRNA viruses that bear a 5′-triphospho-RNA genome, such as influenza virus and RSV, and appears to play a crucial role in the antiviral response to infection with these viruses (138).”
What the sources say
- Not checked yetcites [138] Kato, H., O. Takeuchi, S. Sato, M. Yoneyama, M. Yamamoto, K. Matsui, S. Uematsu, A. Jung, T. Kawai, K. J. Ishii, O. Yamaguchi, K. Otsu, T. Tsujimura, C. S. Koh, C. Reis e Sousa, Y. Matsuura, T. Fujita, and S. Akira. 2006. Differential roles of MDA5 and RIG-I helicases in the recognition of RNA viruses. Nature 441:101-105. [DOI] [PubMed] [Google Scholar]
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“NLRP3 expression and production of IL-1β are induced in primary human airway epithelial cells in response to influenza A virus infection, but it has yet to be determined whether NLRP3 acts directly as a PRR for viral RNA or if it is activated only indirectly in response to PRR signaling (5).”
What the sources say
- Not checked yetcites [5] Allen, I. C., M. A. Scull, C. B. Moore, E. K. Holl, E. McElvania-TeKippe, D. J. Taxman, E. H. Guthrie, R. J. Pickles, and J. P. Ting. 2009. The NLRP3 inflammasome mediates in vivo innate immunity to influenza A virus through recognition of viral RNA. Immunity 30:556-565. [DOI] [PMC free article] [PubMed] [Google Scholar]
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“IFN-α and IFN-β were among the first antiviral agents to be characterized and are still seen as central to the early antiviral response of virus-infected cells.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“It prevents entry of virus into the host cell, either by blocking cellular receptors or by direct binding to virus particles (290).”
What the sources say
- Not checked yetcites [290] Van der Strate, B. W., L. Beljaars, G. Molema, M. C. Harmsen, and D. K. Meijer. 2001. Antiviral activities of lactoferrin. Antiviral Res. 52:225-239. [DOI] [PubMed] [Google Scholar]
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It may state two separate claims as one.
In the paper
“MDA5 has been shown to detect small RNA viruses such as rhinoviruses and is critical in regulating IFN-β, IFN-λ, and proinflammatory cytokine transcription (138).”
What the sources say
- Not checked yetcites [138] Kato, H., O. Takeuchi, S. Sato, M. Yoneyama, M. Yamamoto, K. Matsui, S. Uematsu, A. Jung, T. Kawai, K. J. Ishii, O. Yamaguchi, K. Otsu, T. Tsujimura, C. S. Koh, C. Reis e Sousa, Y. Matsuura, T. Fujita, and S. Akira. 2006. Differential roles of MDA5 and RIG-I helicases in the recognition of RNA viruses. Nature 441:101-105. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This defective IFN response may promote susceptibility to infection by impairing the ability of the infected host cell to undergo early apoptosis and by allowing increased virus replication and, ultimately, cytolysis of infected cells.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Four hBDs (hBD-1 to -4) for airway mucosal defense have been identified in respiratory epithelial cells, but only hBD-2 and hBD-3 act against respiratory viruses (52, 73, 148, 267, 324).”
What the sources say
- Not checked yetcites [52] Doss, M., M. R. White, T. Tecle, D. Gantz, E. C. Crouch, G. Jung, P. Ruchala, A. J. Waring, R. I. Lehrer, and K. L. Hartshorn. 2009. Interactions of alpha-, beta-, and theta-defensins with influenza A virus and surfactant protein D. J. Immunol. 182:7878-7887. [DOI] [PubMed] [Google Scholar]
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plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Data for humans show that increased exhaled nitric oxide after rhinovirus infection is correlated with reduced airway hyperresponsiveness in asthmatic patients, suggesting a beneficial effect of NO in virus-induced asthma exacerbations (42).”
What the sources say
- Not checked yetcites [42] de Gouw, H. W., K. Grunberg, R. Schot, A. C. Kroes, E. C. Dick, and P. J. Sterk. 1998. Relationship between exhaled nitric oxide and airway hyperresponsiveness following experimental rhinovirus infection in asthmatic subjects. Eur. Respir. J. 11:126-132. [DOI] [PubMed] [Google Scholar]
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Activation of NF-κB is common to many respiratory viruses, as demonstrated for rhinovirus (129, 203), RSV (24), and influenza virus (145).”
What the sources say
- Not checked yetcites [129] Johnston, S. L., A. Papi, P. J. Bates, J. G. Mastronarde, M. M. Monick, and G. W. Hunninghake. 1998. Low grade rhinovirus infection induces a prolonged release of IL-8 in pulmonary epithelium. J. Immunol. 160:6172-6181. [PubMed] [Google Scholar]
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boosteddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“The importance of nitric oxide production in antiviral defense of the airway epithelium is demonstrated by studies showing that increased virus (parainfluenza virus 3) replication in airway epithelial cells from CF patients is due at least partly to a lack of NOS-2 induction in response to virus and that NO donor or NOS-2 overexpression provides protection from virus infection (333, 334).”
What the sources say
- Not checked yetcites [333] Zheng, S., B. P. De, S. Choudhary, S. A. Comhair, T. Goggans, R. Slee, B. R. Williams, J. Pilewski, S. J. Haque, and S. C. Erzurum. 2003. Impaired innate host defense causes susceptibility to respiratory virus infections in cystic fibrosis. Immunity 18:619-630. [DOI] [PubMed] [Google Scholar]
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boosteddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“NOS-2 is induced and NO production increased after infection with respiratory viruses (136, 191, 246, 287).”
What the sources say
- Not checked yetcites [136] Kao, Y. J., P. A. Piedra, G. L. Larsen, and G. N. Colasurdo. 2001. Induction and regulation of nitric oxide synthase in airway epithelial cells by respiratory syncytial virus. Am. J. Respir. Crit. Care Med. 163:532-539. [DOI] [PubMed] [Google Scholar]
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plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Respiratory epithelial cells produce high levels of NO, as evidenced by detection of NO in exhaled breath and of NO reaction products (e.g., NO2− and NO3−) in bronchoalveolar lavage fluid from human lungs (77).”
What the sources say
- Not checked yetcites [77] Gaston, B., J. M. Drazen, J. Loscalzo, and J. S. Stamler. 1994. The biology of nitrogen oxides in the airways. Am. J. Respir. Crit. Care Med. 149:538-551. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Bronchial biopsy specimens from subjects undergoing experimental rhinovirus infection show T-cell infiltration of the airway epithelium (69).”
What the sources say
- Not checked yetcites [69] Fraenkel, D. J., P. G. Bardin, G. Sanderson, F. Lampe, S. L. Johnston, and S. T. Holgate. 1995. Lower airways inflammation during rhinovirus colds in normal and in asthmatic subjects. Am. J. Respir. Crit. Care Med. 151:879-886. [DOI] [PubMed] [Google Scholar]
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“RSV strains have also been documented to induce different patterns and severities of inflammatory responses (173, 174, 271).”
What the sources say
- Not checked yetcites [173] McNamara, P. S., B. F. Flanagan, C. A. Hart, and R. L. Smyth. 2005. Production of chemokines in the lungs of infants with severe respiratory syncytial virus bronchiolitis. J. Infect. Dis. 191:1225-1232. [DOI] [PubMed] [Google Scholar]
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plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Airway epithelial cells have been shown to enhance cDC migration into the epithelium via MIP-3α/CCL20 production (232), and MIP-3α/CCL20 induction has been demonstrated in several viral infections, such as influenza virus infection (178, 308).”
What the sources say
- Not checked yetcites [232] Reibman, J., Y. Hsu, L. C. Chen, B. Bleck, and T. Gordon. 2003. Airway epithelial cells release MIP-3alpha/CCL20 in response to cytokines and ambient particulate matter. Am. J. Respir. Cell Mol. Biol. 28:648-654. [DOI] [PubMed] [Google Scholar]
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boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“However, upon extrinsic and intrinsic stimuli such as viral infections, this complex regulatory mechanism is lost or shifts and proinflammatory immune responses are initiated (113, 301).”
What the sources say
- Not checked yetcites [113] Holt, P. G., D. H. Strickland, M. E. Wikstrom, and F. L. Jahnsen. 2008. Regulation of immunological homeostasis in the respiratory tract. Nat. Rev. Immunol. 8:142-152. [DOI] [PubMed] [Google Scholar]
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plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In contrast to cDCs, pDCs are not efficient antigen-presenting cells. Rather, their antiviral action is mediated by production of large amounts of IFN-α, which delivers a powerful innate response to limit viral replication.”
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Upon viral infection, pDCs are recruited rapidly from the bone marrow, and within several days, they form the majority of DCs in the lung (300).”
What the sources say
- Not checked yetcites [300] Wang, H., N. Peters, and J. Schwarze. 2006. Plasmacytoid dendritic cells limit viral replication, pulmonary inflammation, and airway hyperresponsiveness in respiratory syncytial virus infection. J. Immunol. 177:6263-6270. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For instance, studies of mice presensitized by recombinant vaccinia viruses showed that after RSV infection, animals exhibiting mainly Th2 cytokine responses developed enhanced disease with severe symptoms, whereas those with Th1 responses had reduced immunopathology and enhanced viral clearance (6).”
What the sources say
- Not checked yetcites [6] Alwan, W. H., W. J. Kozlowska, and P. J. Openshaw. 1994. Distinct types of lung disease caused by functional subsets of antiviral T cells. J. Exp. Med. 179:81-89. [DOI] [PMC free article] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The appearance of antigen-specific effector T cells in the airways is observed around 6 to 7 days after infection with influenza and parainfluenza viruses (275).”
What the sources say
- Not checked yetcites [275] Swain, S. L., R. W. Dutton, and D. L. Woodland. 2004. T cell responses to influenza virus infection: effector and memory cells. Viral Immunol. 17:197-209. [DOI] [PubMed] [Google Scholar]
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“For instance, pandemic influenza viruses, including H5N1 avian influenza virus and the H1N1 2009 California influenza virus strain, have been associated with more severe inflammation than seasonal influenza virus strains, and it is believed that the magnitude of inflammation is a major contributing factor to disease severity (17, 200, 209, 283, 319).”
What the sources say
- Not checked yetcites [17] Bellani, G., L. Guerra, A. Pesenti, and C. Messa. 2010. Imaging of lung inflammation during severe influenza A: H1N1. Intensive Care Med. 36:717-718. [DOI] [PMC free article] [PubMed] [Google Scholar]
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hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“NK cells also play an important role in the innate immune response against respiratory viruses, with their function being the elimination of a variety of target cells, including virus-infected cells, and the modulation of adaptive immunity toward an efficient antiviral response (22).”
What the sources say
- Not checked yetcites [22] Biron, C. A., K. B. Nguyen, G. C. Pien, L. P. Cousens, and T. P. Salazar-Mather. 1999. Natural killer cells in antiviral defense: function and regulation by innate cytokines. Annu. Rev. Immunol. 17:189-220. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Similarly, rhinovirus group C strains are thought to be associated with increased inflammation and morbidity compared with rhinovirus group A or B strains (10, 125).”
What the sources say
- Not checked yetcites [10] Arden, K. E., C. E. Faux, N. T. O'Neill, P. McErlean, A. Nitsche, S. B. Lambert, M. D. Nissen, T. P. Sloots, and I. M. Mackay. 2010. Molecular characterization and distinguishing features of a novel human rhinovirus (HRV) C, HRVC-QCE, detected in children with fever, cough and wheeze during 2003. J. Clin. Virol. 47:219-223. [DOI] [PMC free article] [PubMed] [Google Scholar]
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hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Airway epithelial cells induce migration of Th1 cells into the mucosa via production of RANTES/CCL5 and IP-10/CXCL10 and that of Th2 cells via production of IL-1β (178).”
What the sources say
- Not checked yetcites [178] Message, S. D., and S. L. Johnston. 2004. Host defense function of the airway epithelium in health and disease: clinical background. J. Leukoc. Biol. 75:5-17. [DOI] [PMC free article] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Airway epithelial cells not only mediate innate immune responses but also regulate adaptive immune responses through interactions with DCs and T and B lymphocytes.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
In the paper
“Interestingly, however, inhibition of neutrophil recruitment to the lung had no effect on virus clearance in a mouse model of influenza virus infection, suggesting only a minor role of neutrophils in this model of respiratory viral infection (309).”
What the sources say
- Not checked yetcites [309] Wareing, M. D., A. L. Shea, C. A. Inglis, P. B. Dias, and S. R. Sarawar. 2007. CXCR2 is required for neutrophil recruitment to the lung during influenza virus infection, but is not essential for viral clearance. Viral Immunol. 20:369-378. [DOI] [PubMed] [Google Scholar]
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Using in vitro culture systems, some differences between susceptibilities to rhinovirus infection have been noted, with bronchial epithelium generating higher viral loads and more expression of virus-inducible mediators than those in bronchial epithelial cells cultured in the same manner (163).”
What the sources say
- Not checked yetcites [163] Lopez-Souza, N., S. Favoreto, H. Wong, T. Ward, S. Yagi, D. Schnurr, W. E. Finkbeiner, G. M. Dolganov, J. H. Widdicombe, H. A. Boushey, and P. C. Avila. 2009. In vitro susceptibility to rhinovirus infection is greater for bronchial than for nasal airway epithelial cells in human subjects. J. Allergy Clin. Immunol. 123:1384-1390. [DOI] [PMC free article] [PubMed] [Google Scholar]
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Whereas rhinovirus-induced cytotoxicity was shown in bronchial epithelial cells after rhinovirus infection (27)”
What the sources say
- Not checked yetcites [27] Bossios, A., S. Psarras, D. Gourgiotis, C. L. Skevaki, A. G. Constantopoulos, P. Saxoni-Papageorgiou, and N. G. Papadopoulos. 2005. Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells. Respir. Res. 6:114. [DOI] [PMC free article] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Cytotoxicity upon infection with certain viruses may depend on the virus strain, infection conditions, and infected cell type and density (27).”
What the sources say
- Not checked yetcites [27] Bossios, A., S. Psarras, D. Gourgiotis, C. L. Skevaki, A. G. Constantopoulos, P. Saxoni-Papageorgiou, and N. G. Papadopoulos. 2005. Rhinovirus infection induces cytotoxicity and delays wound healing in bronchial epithelial cells. Respir. Res. 6:114. [DOI] [PMC free article] [PubMed] [Google Scholar]
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We further discuss how vRTIs can lead to perturbed inflammatory responses and to increased mucus production, which will be detrimental rather than protective to the host.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, considering that the airway epithelium is the main site of viral infection, it is likely to contribute significantly to the type and magnitude of the inflammatory response.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
- Rests on an assumption: The airway epithelium is the main site of viral infection.
In the paper
“For instance, TGF-β increases airway wound repair through MMP-2 upregulation (154).”
What the sources say
- Not checked yetcites [154] Lechapt-Zalcman, E., V. Pruliere-Escabasse, D. Advenier, S. Galiacy, C. Charriere-Bertrand, A. Coste, A. Harf, M. P. d'Ortho, and E. Escudier. 2006. Transforming growth factor-beta1 increases airway wound repair via MMP-2 upregulation: a new pathway for epithelial wound repair? Am. J. Physiol. Lung Cell. Mol. Physiol. 290:L1277-L1282. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Migrating basal airway epithelial cells repopulate damaged areas, proliferate, and differentiate until epithelial integrity has been restored (242).”
What the sources say
- Not checked yetcites [242] Sacco, O., M. Silvestri, F. Sabatini, R. Sale, A. C. Defilippi, and G. A. Rossi. 2004. Epithelial cells and fibroblasts: structural repair and remodelling in the airways. Paediatr. Respir. Rev. 5(Suppl. A):S35-S40. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“MMPs play a crucial role in the remodeling of the matrix onto which cells migrate, and many pathways are involved in this process (294).”
What the sources say
- Not checked yetcites [294] Visse, R., and H. Nagase. 2003. Matrix metalloproteinases and tissue inhibitors of metalloproteinases: structure, function, and biochemistry. Circ. Res. 92:827-839. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Most viruses have efficient ways to inhibit IFN synthesis, to bind and inactivate secreted IFN molecules, to block IFN-activated signaling, or to disturb the action of IFN-induced antiviral proteins.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“It is currently believed that NS2 prevents RIG-I signaling by interfering with the RIG-I-MAVS interaction, therefore severely limiting signaling mediated by the critical interaction between the sensor RIG-I and its specific adaptor, MAVS (161).”
What the sources say
- Not checked yetcites [161] Ling, Z., K. C. Tran, and M. N. Teng. 2009. Human respiratory syncytial virus nonstructural protein NS2 antagonizes the activation of beta interferon transcription by interacting with RIG-I. J. Virol. 83:3734-3742. [DOI] [PMC free article] [PubMed] [Google Scholar]
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“V proteins may be expressed at high levels during the initial stages of infection and therefore limit IRF3 activation by binding IKK-ɛ and preventing IRF-3 activation, and hence IFN induction (165).”
What the sources say
- Not checked yetcites [165] Lu, L. L., M. Puri, C. M. Horvath, and G. C. Sen. 2008. Select paramyxoviral V proteins inhibit IRF3 activation by acting as alternative substrates for inhibitor of kappaB kinase epsilon (IKKe)/TBK1. J. Biol. Chem. 283:14269-14276. [DOI] [PMC free article] [PubMed] [Google Scholar]
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Furthermore, they induce the production of proangiogenic molecules, including amphiregulin (a member of the epidermal growth factor [EGF] family) and vascular endothelial growth factor (VEGF), and therefore may lead to increased angiogenesis (156, 220).”
What the sources say
- Not checked yetcites [156] Leigh, R., W. Oyelusi, S. Wiehler, R. Koetzler, R. S. Zaheer, R. Newton, and D. Proud. 2008. Human rhinovirus infection enhances airway epithelial cell production of growth factors involved in airway remodeling. J. Allergy Clin. Immunol. 121:1238-1245. [DOI] [PubMed] [Google Scholar]
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hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The NS1 and NS2 proteins of RSV inhibit STAT-2 activation, thus blocking IFN-α/β function (161, 162).”
What the sources say
- Not checked yetcites [161] Ling, Z., K. C. Tran, and M. N. Teng. 2009. Human respiratory syncytial virus nonstructural protein NS2 antagonizes the activation of beta interferon transcription by interacting with RIG-I. J. Virol. 83:3734-3742. [DOI] [PMC free article] [PubMed] [Google Scholar]
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plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“A role for airway epithelial cells in contributing to the Th2 phenotype is possible, as they have receptors for and respond to IL-4, IL-13, and IL-25 (68, 115).”
What the sources say
- Not checked yetcites [68] Fort, M. M., J. Cheung, D. Yen, J. Li, S. M. Zurawski, S. Lo, S. Menon, T. Clifford, B. Hunte, R. Lesley, T. Muchamuel, S. D. Hurst, G. Zurawski, M. W. Leach, D. M. Gorman, and D. M. Rennick. 2001. IL-25 induces IL-4, IL-5, and IL-13 and Th2-associated pathologies in vivo. Immunity 15:985-995. [DOI] [PubMed] [Google Scholar]
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plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In allergic asthmatic subjects, Th1 responses to rhinovirus are downregulated, as indicated by lower levels of IL-12 and IFN-γ, whereas Th2 responses are increased, with higher levels of IL-4, IL-5, and IL-13 (179).”
What the sources say
- Not checked yetcites [179] Message, S. D., V. Laza-Stanca, P. Mallia, H. L. Parker, J. Zhu, T. Kebadze, M. Contoli, G. Sanderson, O. M. Kon, A. Papi, P. K. Jeffery, L. A. Stanciu, and S. L. Johnston. 2008. Rhinovirus-induced lower respiratory illness is increased in asthma and related to virus load and Th1/2 cytokine and IL-10 production. Proc. Natl. Acad. Sci. U. S. A. 105:13562-13567. [DOI] [PMC free article] [PubMed] [Google Scholar]
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Furthermore, RSV and rhinovirus can lead to induction of the pro-Th2 cytokine TSLP, suggesting a direct link between viral infection of the epithelium and an altered immune response toward a Th2 pattern (4, 157, 264).”
What the sources say
- Not checked yetcites [4] Allakhverdi, Z., M. R. Comeau, H. K. Jessup, B. R. Yoon, A. Brewer, S. Chartier, N. Paquette, S. F. Ziegler, M. Sarfati, and G. Delespesse. 2007. Thymic stromal lymphopoietin is released by human epithelial cells in response to microbes, trauma, or inflammation and potently activates mast cells. J. Exp. Med. 204:253-258. [DOI] [PMC free article] [PubMed] [Google Scholar]
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hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This is illustrated by studies showing that influenza virus infection results in decreased tracheal mucociliary velocity and clearance of S. pneumoniae (172, 213).”
What the sources say
- Not checked yetcites [172] McCullers, J. A., A. R. Iverson, R. McKeon, and P. J. Murray. 2008. The platelet activating factor receptor is not required for exacerbation of bacterial pneumonia following influenza. Scand. J. Infect. Dis. 40:11-17. [DOI] [PMC free article] [PubMed] [Google Scholar]
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plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For instance, rhinoviruses disrupt airway epithelial barrier functions and promote the paracellular migration of bacteria such as H. influenzae (244).”
What the sources say
- Not checked yetcites [244] Sajjan, U., Q. Wang, Y. Zhao, D. C. Gruenert, and M. B. Hershenson. 2008. Rhinovirus disrupts the barrier function of polarized airway epithelial cells. Am. J. Respir. Crit. Care Med. 178:1271-1281. [DOI] [PMC free article] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In addition, perturbation of the epithelial barrier upon virus infection may increase paracellular permeability and facilitate translocation of bacteria and their soluble products into the submucosa.”
What the sources say
- Not checked yetcites [244] Sajjan, U., Q. Wang, Y. Zhao, D. C. Gruenert, and M. B. Hershenson. 2008. Rhinovirus disrupts the barrier function of polarized airway epithelial cells. Am. J. Respir. Crit. Care Med. 178:1271-1281. [DOI] [PMC free article] [PubMed] [Google Scholar]
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Mechanisms involved in ciliostasis are poorly understood but could be mediated by ion alterations during viral attachment and replication, by direct damage to the ciliary system, or by damage through the induction of NO, cyclic AMP, calmodulin, and inositol 1,4,5-triphosphate (InP3) production, which alters baseline ciliary beat frequency (33) or modulates hfh4 and mdnh5 gene expression, resulting”
What the sources say
- Not checked yetcites [33] Chilvers, M. A., and C. O'Callaghan. 2000. Local mucociliary defence mechanisms. Paediatr. Respir. Rev. 1:27-34. [DOI] [PubMed] [Google Scholar]
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hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“It also increases the expression of ICAM-1, which serves as a receptor both for itself and for H. influenzae (11, 316).”
What the sources say
- Not checked yetcites [11] Avadhanula, V., C. A. Rodriguez, J. P. Devincenzo, Y. Wang, R. J. Webby, G. C. Ulett, and E. E. Adderson. 2006. Respiratory viruses augment the adhesion of bacterial pathogens to respiratory epithelium in a viral species- and cell type-dependent manner. J. Virol. 80:1629-1636. [DOI] [PMC free article] [PubMed] [Google Scholar] source
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plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For instance, whereas RSV upregulates cellular receptors such as ICAM-1 and CEACAM-1, leading to an increase of bacterial adherence, influenza virus has no effect on the expression of these receptors (11).”
What the sources say
- Not checked yetcites [11] Avadhanula, V., C. A. Rodriguez, J. P. Devincenzo, Y. Wang, R. J. Webby, G. C. Ulett, and E. E. Adderson. 2006. Respiratory viruses augment the adhesion of bacterial pathogens to respiratory epithelium in a viral species- and cell type-dependent manner. J. Virol. 80:1629-1636. [DOI] [PMC free article] [PubMed] [Google Scholar] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Increased bacterial adherence facilitates biofilm formation and could represent a critical step in permanent airway colonization by P. aeruginosa in cystic fibrosis patients (98).”
What the sources say
- Not checked yetcites [98] Hassett, D. J., T. R. Korfhagen, R. T. Irvin, M. J. Schurr, K. Sauer, G. W. Lau, M. D. Sutton, H. Yu, and N. Hoiby. 2010. Pseudomonas aeruginosa biofilm infections in cystic fibrosis: insights into pathogenic processes and treatment strategies. Expert Opin. Ther. Targets 14:117-130. [DOI] [PubMed] [Google Scholar]
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, virus-induced cell death may expose new receptors for bacterial adherence or impair mechanical removal of attached pathogens (30, 41, 96).”
What the sources say
- Not checked yetcites [30] Bragonzi, A., E. Copreni, S. de Bentzmann, M. Ulrich, and M. Conese. 2004. Airway epithelial cell-pathogen interactions. J. Cyst. Fibros. 3(Suppl. 2):197-201. [DOI] [PubMed] [Google Scholar]
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hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Mechanisms responsible for the increased adherence to respiratory epithelial cells differ between viruses and also between cell types.”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, steroids are well established as suppressors of viral (56, 268, 296) and bacterial (100) inflammation and mucin production and may modulate epithelial damage, injury, and repair.”
What the sources say
- Not checked yetcites [56] Edwards, M. R., M. W. Johnson, and S. L. Johnston. 2006. Combination therapy: synergistic suppression of virus-induced chemokines in airway epithelial cells. Am. J. Respir. Cell Mol. Biol. 34:616-624. [DOI] [PubMed] [Google Scholar]
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boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Impairment of TLR4 and TLR5 has been demonstrated after influenza virus infection, leading to reduced neutrophil recruitment and increased P. aeruginosa and S. pneumoniae adherence in airway epithelial cells (46).”
What the sources say
- Not checked yetcites [46] Didierlaurent, A., J. Goulding, S. Patel, R. Snelgrove, L. Low, M. Bebien, T. Lawrence, L. S. van Rijt, B. N. Lambrecht, J. C. Sirard, and T. Hussell. 2008. Sustained desensitization to bacterial Toll-like receptor ligands after resolution of respiratory influenza infection. J. Exp. Med. 205:323-329. [DOI] [PMC free article] [PubMed] [Google Scholar]
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“They lead to more than 400,000 hospitalizations per year among children in the United States and are therefore a major burden on the health care system (105, 180, 194).”
What the sources say
- Not checked yetcites [105] Henrickson, K. J., S. Hoover, K. S. Kehl, and W. Hua. 2004. National disease burden of respiratory viruses detected in children by polymerase chain reaction. Pediatr. Infect. Dis. J. 23:S11-S18. [DOI] [PubMed] [Google Scholar]
- Not checked yetcites [180] Mizgerd, J. P. 2006. Lung infection—a public health priority. PLoS Med. 3:e76. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Not checked yetcites [194] Nair, H., D. J. Nokes, B. D. Gessner, M. Dherani, S. A. Madhi, R. J. Singleton, K. L. O'Brien, A. Roca, P. F. Wright, N. Bruce, A. Chandran, E. Theodoratou, A. Sutanto, E. R. Sedyaningsih, M. Ngama, P. K. Munywoki, C. Kartasasmita, E. A. Simoes, I. Rudan, M. W. Weber, and H. Campbell. 2010. Global burden of acute lower respiratory infections due to respiratory syncytial virus in young children: a systematic review and meta-analysis. Lancet 375:1545-1555. [DOI] [PMC free article] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“A recent study demonstrated effectiveness of the ketomacrolide telithromycin in asthma exacerbations (128).”
What the sources say
- Not checked yetcites [128] Johnston, S. L., F. Blasi, P. N. Black, R. J. Martin, D. J. Farrell, and R. B. Nieman. 2006. The effect of telithromycin in acute exacerbations of asthma. N. Engl. J. Med. 354:1589-1600. [DOI] [PubMed] [Google Scholar]
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“a recent study found no protective effect of the above in a trial of post-RSV bronchiolitis in children (23).”
What the sources say
- Not checked yetcites [23] Bisgaard, H., A. Flores-Nunez, A. Goh, P. Azimi, A. Halkas, M. P. Malice, J. L. Marchal, S. B. Dass, T. F. Reiss, and B. A. Knorr. 2008. Study of montelukast for the treatment of respiratory symptoms of post-respiratory syncytial virus bronchiolitis in children. Am. J. Respir. Crit. Care Med. 178:854-860. [DOI] [PubMed] [Google Scholar]
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“By use of in vitro culture systems, azithromycin was able to augment rhinovirus-induced IFNs and their inducible genes and to decrease virus replication (81).”
What the sources say
- Not checked yetcites [81] Gielen, V., S. L. Johnston, and M. R. Edwards. 2010. Azithromycin induces anti-viral responses in bronchial epithelial cells. Eur. Respir. J. 36:646-654. [DOI] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“vRTIs are an important cause of morbidity and, in some cases, mortality.”
What the sources say
- Not checked yetcites [105] Henrickson, K. J., S. Hoover, K. S. Kehl, and W. Hua. 2004. National disease burden of respiratory viruses detected in children by polymerase chain reaction. Pediatr. Infect. Dis. J. 23:S11-S18. [DOI] [PubMed] [Google Scholar]
- Not checked yetcites [180] Mizgerd, J. P. 2006. Lung infection—a public health priority. PLoS Med. 3:e76. [DOI] [PMC free article] [PubMed] [Google Scholar]
- Not checked yetcites [194] Nair, H., D. J. Nokes, B. D. Gessner, M. Dherani, S. A. Madhi, R. J. Singleton, K. L. O'Brien, A. Roca, P. F. Wright, N. Bruce, A. Chandran, E. Theodoratou, A. Sutanto, E. R. Sedyaningsih, M. Ngama, P. K. Munywoki, C. Kartasasmita, E. A. Simoes, I. Rudan, M. W. Weber, and H. Campbell. 2010. Global burden of acute lower respiratory infections due to respiratory syncytial virus in young children: a systematic review and meta-analysis. Lancet 375:1545-1555. [DOI] [PMC free article] [PubMed] [Google Scholar]
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“While a recent study demonstrated that children admitted to hospital with asthma-related symptoms were less likely to have used therapies, including leukotriene receptor antagonists (127)”
What the sources say
- Not checked yetcites [127] Johnston, N. W., S. L. Johnston, J. M. Duncan, J. M. Greene, T. Kebadze, P. K. Keith, M. Roy, S. Waserman, and M. R. Sears. 2005. The September epidemic of asthma exacerbations in children: a search for etiology. J. Allergy Clin. Immunol. 115:132-138. [DOI] [PMC free article] [PubMed] [Google Scholar]
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, respiratory viruses have evolved strategies to subvert epithelial defense mechanisms and can lead to complications such as loss of epithelial integrity, perturbed inflammatory responses, increased mucus production, and secondary bacterial infections.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
The paper relies on this without support.
The airway epithelium is the main site of viral infection.
“However, considering that the airway epithelium is the main site of viral infection, it is likely to contribute significantly to the type and magnitude of the inflammatory response.”
The paper relies on this without support.
The physiochemical characteristics of the upper (nasal) and lower (bronchial) epithelia are very similar.
“The general consensus is that the physiochemical characteristics of the upper (nasal) and lower (bronchial) epithelia are very similar”
The paper relies on this without support.
The airway epithelium plays an important role as a protective physical and functional barrier between the external environment and underlying tissues and as a central element in the initiation and regulation of innate and adaptive immune responses in the lung.
“The airway epithelium plays an important role as a protective physical and functional barrier between the external environment and underlying tissues and as a central element in the initiation and regulation of innate and adaptive immune responses in the lung.”
The paper relies on this without support.
Airway epithelial cells are the principal hosts for respiratory viruses.
“Airway epithelial cells are the principal hosts for respiratory viruses.”
The paper relies on this without support.
Apoptosis acts as a protective mechanism to limit replication and spread of the virus to other cells, but exaggerated apoptosis can lead to a loss of integrity and protection of the epithelium, with detrimental consequences.
“Apoptosis acts as a protective mechanism to limit replication and spread of the virus to other cells, but exaggerated apoptosis can lead to a loss of integrity and protection of the epithelium, with detrimental consequences.”
The paper relies on this without support.
Epithelial repair initiates quickly after injury.
“Epithelial repair initiates quickly after injury.”
The paper relies on this without support.
Mucus contains many components that bind bacteria.
“Mucus contains many components that bind bacteria.”
The paper relies on this without support.
Most respiratory viral infections are self-limited and associated with minor morbidity.
“Fortunately, most respiratory viral infections are self-limited and associated with minor morbidity.”
The paper relies on this without support.
A frequent point of interference by viruses is the Jak-STAT signaling pathway, used by IFNs to induce transcription of antiviral genes.
“A frequent point of interference by viruses is the Jak-STAT signaling pathway, used by IFNs to induce transcription of antiviral genes.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“First, mucus production in the respiratory tract is increased to facilitate viral clearance during infections. However, excessive mucus production can lead to airway obstruction by impeding mucociliary clearance (125).”
From Respiratory viral infection-induced microbiome alterations and secondary bacterial pneumonia. (2018) · cites this paper as [125]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ INTRODUCTION
“bronchial epithelium generating higher viral loads and more expression of virus-inducible mediators than those in bronchial epithelial cells cultured in the same manner (163).”
§ REFERENCES
“163.Lopez-Souza, N., S. Favoreto, H. Wong, T. Ward, S. Yagi, D. Schnurr, W. E. Finkbeiner, G. M. Dolganov, J. H. Widdicombe, H. A. Boushey, and P. C. Avila. 2009. In vitro susceptibility to rhinovirus infection is greater for bronchial than for nasal airway epithelial cells in human subjects.”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ INTRODUCTION
“Studies on bacterial adherence to human respiratory epithelial cells during viral infection”
§ INTRODUCTION
“2010 ( 213 ) Influenza virus S. pneumoniae Murine tracheal explants”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ INTRODUCTION
“RV, rhinovirus; HPIV-3, human metapneumovirus type 3.”
§ REFERENCES
“332.Zhang, L., A. Bukreyev, C. I. Thompson, B. Watson, M. E. Peeples, P. L. Collins, and R. J. Pickles. 2005. Infection of ciliated cells by human parainfluenza virus type 3 in an in vitro model of human airway epithelium.”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ INTRODUCTION
“TLR7, TLR8, and TLR9 recognize double-stranded RNA (dsRNA), single-stranded RNA (ssRNA), and CpG DNA, respectively (141).”
§ INTRODUCTION
“pDCs typically express TLR7 and TLR9, recognizing single-stranded RNA and viral DNA”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ INTRODUCTION
“1982 ( 131 ) Influenza virus S. pneumoniae Mouse tracheal tissue”
§ REFERENCES
“131.Jones, W. T., and J. H. Menna. 1982. Influenza type A virus-mediated adherence of type 1a group B streptococci to mouse tracheal tissue in vivo.”
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Metadata
- Authors
- Vareille, M., Kieninger, E., Edwards, M. R., & Regamey, N.
- Affiliations
- Division of Respiratory Medicine, Department of Pediatrics, University Children's Hospital of Bern, Inselpital, 3010 Bern, Switzerland
- University of Bern (CH)
- Asthma UK (GB)
- Venue
- Clinical Microbiology Reviews
- Publisher
- American Society for Microbiology
- Published
- 2011-01
- Volume
- 24
- Issue
- 1
- Pages
- 210-229
- ISSN
- 0893-8512 (ISSN-L)
- 1098-6618
- PMC
- PMC3021210
- OpenAlex
- W2145181045
- Semantic Scholar
- a942a5a52b73a1f1befb07f36f25743cfed15229
- Cited by
- 655
- References
- 341
- Citations by year
- 2026: 25 · 2025: 39 · 2024: 40 · 2023: 57 · 2022: 44 · 2021: 64 · 2020: 52 · 2019: 36 · 2018: 36 · 2017: 45 · 2016: 44 · 2015: 49 · 2014: 48 · 2013: 47 · 2012: 21
- FWCI
- 3.55
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinical Microbiology Reviews (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Bern Open Repository and Information System (University of Bern) (submittedVersion)
- Funders
- National Institute for Health and Care Research (NF-SI-0508-10212)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- airway epithelium, respiratory viruses, innate immunity, interferon, lactoferrin, beta-defensins, nitric oxide, cytokines and chemokines, viral immune evasion, epithelial barrier integrity, mucus hypersecretion, mucostasis, lung injury, viral clearance
- MeSH terms
- Humans, Immunity, Innate, Respiratory Tract Infections, Viruses, Respiratory Mucosa, Adaptive Immunity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-09 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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