Respiratory viral infection-induced microbiome alterations and secondary bacterial pneumonia.

May combine two claims.

Bacterial co-infection was detected in ~30% of cases in the 2009 H1N1 pandemic, with high mortality rates despite administration of appropriate antibiotics.

“Bacterial co-infection was also detected in ~30% of cases in the 2009 H1N1 pandemic, with high mortality rates despite administration of appropriate antibiotics”

• cites [11] Cillóniz, 2012, Bacterial co-infection with H1N1 infection in patients admitted with community acquired pneumonia, J Infect sourceNot checked yet

  Not checked in the free run.

• cites [12] Gill, 2010, Pulmonary pathologic findings of fatal 2009 pandemic influenza A/H1N1 viral infections, Arch Pathol Lab Med sourceNot checked yet

  Not checked in the free run.

• cites [13] Jain, 2009, Hospitalized patients with 2009 H1N1 influenza in the United States, April-June 2009, N Engl J Med sourceNot checked yet

  Not checked in the free run.

• cites [14] Kumar, 2009, Critically ill patients with 2009 influenza A(H1N1) infection in Canada, JAMA sourceNot checked yet

  Not checked in the free run.

• cites [15] Martín-Loeches, 2011, Community-acquired respiratory coinfection in critically ill patients with pandemic 2009 influenza A(H1N1) virus, Chest sourceNot checked yet

  Not checked in the free run.

• cites [16] Palacios, 2009, Streptococcus pneumoniae coinfection is correlated with the severity of H1N1 pandemic influenza, PLoS ONE sourceNot checked yet

  Not checked in the free run.

• cites [17] Shieh, 2010, 2009 pandemic influenza A (H1N1): pathology and pathogenesis of 100 fatal cases in the United States, Am J Pathol sourceNot checked yet

  Not checked in the free run.

• cites [18] Domínguez-Cherit, 2009, Critically Ill patients with 2009 influenza A(H1N1) in Mexico, JAMA sourceNot checked yet

  Not checked in the free run.

May combine two claims.

These dysbiotic changes may alter subsequent immune function against secondary bacterial infection or alter the dynamics of inter-microbial interactions, thereby enhancing the proliferation of potentially pathogenic bacterial species.

“which in turn may alter subsequent immune function against secondary bacterial infection or alter the dynamics of inter-microbial interactions, thereby enhancing the proliferation of potentially pathogenic bacterial species”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

The 1918-1919 H1N1 influenza pandemic resulted in more than 50 million deaths, with many caused by bacterial super-infection leading to secondary pneumonia.

“the so-called “Spanish Flu” pandemic of H1N1 influenza A virus from 1918 to 1919 resulted in more than 50 million deaths, with many caused by bacterial super-infection leading to secondary pneumonia”

• cites [1] Brundage, 2006, Interactions between influenza and bacterial respiratory pathogens: implications for pandemic preparedness, Lancet Infect Dis sourceNot checked yet

  Not checked in the free run.

• cites [2] Chien, 2009, Bacterial pathogens and death during the 1918 influenza pandemic, N Engl J Med sourceNot checked yet

  Not checked in the free run.

• cites [3] Johnson, 2002, Updating the accounts: global mortality of the 1918-1920 “Spanish” influenza pandemic, Bull Hist Med sourceNot checked yet

  Not checked in the free run.

• cites [4] McCullers, 2006, Insights into the interaction between influenza virus and pneumococcus, Clin Microbiol Rev sourceNot checked yet

  Not checked in the free run.

• cites [5] Morens, 2007, The 1918 influenza pandemic: insights for the 21st century, J Infect Dis sourceNot checked yet

  Not checked in the free run.

• cites [6] Morens, 2008, Predominant role of bacterial pneumonia as a cause of death in pandemic influenza: implications for pandemic influenza preparedness, J Infect Dis sourceNot checked yet

  Not checked in the free run.

• cites [7] The origin and virulence of the 1918 “Spanish” influenza virus86112 TaubenbergerJK 17526158Proc Am Philos Soc1502006Not checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

Secondary bacterial infections following respiratory viral infections often have a more severe clinical course.

“which often have a more severe clinical course”

Probably not a substantial claim: may not pass S4 (based).

Unique microbial communities reside on the mucosal surfaces of the gastrointestinal tract and the respiratory tract.

“unique microbial communities reside on the mucosal surfaces of the gastrointestinal tract and the respiratory tract”

Classified as probably not a substantial claim.

The mechanisms underlying post-viral bacterial infections are complex and include multifactorial processes mediated by interactions between viruses, bacteria, and the host immune system.

“The mechanisms underlying post-viral bacterial infections are complex, and include multifactorial processes mediated by interactions between viruses, bacteria, and the host immune system.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Microbial metabolites are integral for promoting immune responses in the gut against pathogens, including inducing secretion of IL-18 and defensins.

“microbial metabolites are integral for promoting immune responses in the gut against pathogens, including inducing secretion of IL-18 (36) and defensins (37, 38)”

• cites [36] Kalina, 2002, Enhanced production of IL-18 in butyrate-treated intestinal epithelium by stimulation of the proximal promoter region, Eur J Immunol sourceNot checked yet

  Not checked in the free run.

• cites [37] Schauber, 2003, Expression of the cathelicidin LL-37 is modulated by short chain fatty acids in colonocytes: relevance of signalling pathways, Gut sourceNot checked yet

  Not checked in the free run.

• cites [38] Schauber, 2004, Histone-deacetylase inhibitors induce the cathelicidin LL-37 in gastrointestinal cells, Mol Immunol sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

SCFAs promote the development of naive CD4+ T cells into regulatory T cells, induce "tolerogenic" dendritic cells in the intestinal mucosa, and limit autoimmunity.

“SCFAs promote the development of naive CD4+ T cells into regulatory T cells (31, 32), induce “tolerogenic” dendritic cells in the intestinal mucosa (33), and limit autoimmity (34, 35).”

• cites [31] Smith, 2013, The microbial metabolites, short-chain fatty acids, regulate colonic Treg cell homeostasis, Science sourceNot checked yet

  Not checked in the free run.

• cites [32] Arpaia, 2013, Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation, Nature sourceNot checked yet

  Not checked in the free run.

• cites [33] Goverse, 2017, Diet-derived short chain fatty acids stimulate intestinal epithelial cells to induce mucosal tolerogenic dendritic cells, J Immunol sourceNot checked yet

  Not checked in the free run.

• cites [34] Mariño, 2017, Gut microbial metabolites limit the frequency of autoimmune T cells and protect against type 1 diabetes, Nat Immunol sourceNot checked yet

  Not checked in the free run.

• cites [35] Haase, 2018, Impacts of microbiome metabolites on immune regulation and autoimmunity, Immunology sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S4 (based). May combine two claims.

Potential mechanisms by which microbiome changes might modulate susceptibility to secondary bacterial infections include alterations in the nature and magnitude of the immune response in the host and facilitating growth of pathogens in the absence of normal commensals.

“potential mechanisms by which these changes might modulate susceptibility to secondary bacterial infections include alterations in the nature and magnitude of the immune response in the host (microbiome on host effects) and facilitating growth of pathogens in the absence of normal commensals (inter-microbial effects)”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Germ-free mice have markedly underdeveloped gut-associated lymphoid tissues, decreased number and smaller-sized Peyer's patches and mesenteric lymph nodes, and defects in antibody production, compared to specific pathogen free (SPF) mice.

“Germ-free (GF) mice (which lack microbiota) have markedly underdeveloped gut-associated lymphoid tissues, decreased number and smaller-sized Peyer's patches and mesenteric lymph nodes, and defects in antibody production, compared to specific pathogen free (SPF) mice.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Wild-living mice exhibit more diverse microbiomes, with significant abundance of Proteobacteria as well as Firmicutes and Bacteroidetes.

“Wild-living mice exhibit more diverse microbiomes, with significant abundance of Proteobacteria as well as Firmicutes and Bacteroidetes”

• cites [21] Rosshart, 2017, Wild mouse gut microbiota promotes host fitness and improves disease resistance, Cell sourceNot checked yet

  Not checked in the free run.

Classified as probably not a substantial claim.

The effects of these alterations on risk of secondary bacterial pneumonia have not been studied.

“While the effects of these alterations on risk of secondary bacterial pneumonia have not been studied”

Probably not a substantial claim: may not pass S3 (load-bearing).

Germ-free animals exhibit increased susceptibility to multiple types of infections, including viruses, bacteria, and parasites.

“germ-free animals exhibit increased susceptibility to multiple types of infections, including viruses, bacteria, and parasites”

• cites (22,–27)Not checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing).

Short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate are fermentation products of dietary fiber and carbohydrates by large intestinal bacteria.

“short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate are fermentation products of dietary fiber and carbohydrates by large intestinal bacteria”

• cites [30] Cummings, 1983, Fermentation in the human large intestine: evidence and implications for health, Lancet sourceNot checked yet

  Not checked in the free run.

Classified as probably not a substantial claim.

Disruptions in the normal microbial communities by an acute viral infection might contribute to the development of post-viral bacterial pneumonia.

“This raises the possibility that disruptions in the normal microbial communities by an acute viral infection might contribute to the development of post-viral bacterial pneumonia.”

Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.

During health, the human gut bacterial community is diverse, with each individual harboring over 100 trillion bacteria, comprised of over 150 different species.

“During health, the human gut bacterial community is diverse, with each individual harboring over 100 trillion bacteria, comprised of over 150 different species.”

Probably not a substantial claim: may not pass S3 (load-bearing).

The gastrointestinal microbiota is dominated by Firmicutes and Bacteroidetes, with lower abundances of Proteobacteria and Actinobacteria.

“The gastrointestinal microbiota is dominated by Firmicutes (e.g., Lactobacillus, Bacillus, and Clostridium) and Bacteroidetes (e.g., Bacteroides), with lower abundances of Proteobacteria (e.g., Escherichia) and Actinobacteria (e.g., Bifidobacterium)”

• cites [19] Honda, 2012, The microbiome in infectious disease and inflammation, Annu Rev Immunol sourceNot checked yet

  Not checked in the free run.

• cites [20] Human, 2012, Structure, function and diversity of the healthy human microbiome, Nature sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Segmented filamentous bacteria are critical promoters of intestinal mucosal IgA production and Th17 cell induction.

“segmented filamentous bacteria are critical promoters of intestinal mucosal IgA production (39, 40)and Th17 cell induction (41, 42)”

• cites [39] Klaasen, 1993, Apathogenic, intestinal, segmented, filamentous bacteria stimulate the mucosal immune system of mice, Infect Immun sourceNot checked yet

  Not checked in the free run.

• cites [40] Talham, 1999, Segmented filamentous bacteria are potent stimuli of a physiologically normal state of the murine gut mucosal immune system, Infect Immun sourceNot checked yet

  Not checked in the free run.

• cites [41] Ivanov, 2009, Induction of intestinal Th17 cells by segmented filamentous bacteria, Cell sourceNot checked yet

  Not checked in the free run.

• cites [42] Gaboriau-Routhiau, 2009, The key role of segmented filamentous bacteria in the coordinated maturation of gut helper T cell responses, Immunity sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

The gut microbiome plays an integral role in shaping the immune system starting early in life, with continued influence on priming the nature and robustness of immune responses throughout one's lifetime.

“The gut microbiome, in particular, has been shown to play an integral role in shaping the immune system starting early in life, with continued influence on priming the nature and robustness of immune responses throughout one's lifetime.”

May combine two claims.

Compared to free-living mice or laboratory animals exposed to gut flora from wild mice, SPF animals have a more limited microbial community and are also more susceptible to inflammatory diseases, with a reduced immune repertoire including deficits in memory responses.

“compared to free-living mice or laboratory animals exposed to gut flora from wild mice, SPF animals have a more limited microbial community and are also more susceptible to inflammatory diseases, with a reduced immune repertoire including deficits in memory responses”

• cites [21] Rosshart, 2017, Wild mouse gut microbiota promotes host fitness and improves disease resistance, Cell sourceNot checked yet

  Not checked in the free run.

• cites [28] Reese, 2016, Sequential infection with common pathogens promotes human-like immune gene expression and altered vaccine response, Cell Host Microbe sourceNot checked yet

  Not checked in the free run.

• cites [29] Beura, 2016, Normalizing the environment recapitulates adult human immune traits in laboratory mice, Nature sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S4 (based). May combine two claims.

Emerging evidence suggests that microbial communities residing on mucosal surfaces shape the rigor of immune responses and the ecological relationships between host and pathogens.

“emerging evidence suggests that our microbial communities residing on our mucosal surfaces likely shape the rigor of our immune responses and shape the ecological relationships between host and pathogens”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Bacterial metabolites generated by gut commensals contribute to the maintenance of intact epithelial integrity, regulatory T-cell development, and a relatively anti-inflammatory immune state.

“bacterial metabolites generated by gut commensals contribute to the maintenance of intact epithelial integrity, regulatory T-cell development, and a relatively anti-inflammatory immune state”

Probably not a substantial claim: may not pass S4 (based). May combine two claims.

The pathogenesis of super-infection has been attributed to direct mucosal/epithelial damage by influenza virus, increased bacterial colonization of the upper and lower respiratory tracts, and dysregulation of immune responses, which all lead to increased susceptibility to secondary bacterial infections.

“The pathogenesis of super-infection has been attributed to direct mucosal/epithelial damage by influenza virus, increased bacterial colonization of the upper and lower respiratory tracts (URT and LRT, respectively), and dysregulation of immune responses, which all lead to increased susceptibility to secondary bacterial infections.”

May combine two claims.

The effects of viral infection on the respiratory microbiome appear to be relatively modest, but detectable.

“the effects of viral infection on the respiratory microbiome appear to be relatively modest, but detectable”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

The respiratory tract harbors distinct communities of microbes, with multiple discrete ecological niches that vary in temperature, pH, oxygen tension, mucus production, and other factors.

“The respiratory tract also harbors distinct communities of microbes, with multiple discrete ecological niches (e.g., nasal cavity, oropharynx, upper airways) that vary in terms of temperature, pH, oxygen tension, mucus production, and other factors.”

Probably not a substantial claim: may not pass S3 (load-bearing).

The gut microbiome plays an integral role in the development, instruction, and priming of the immune system.

“The gut microbiome, in addition to its metabolic functions in the host, plays an integral role in the development, instruction, and priming of the immune system.”

May combine two claims.

The increase in Proteobacteria appears to be mediated by type I interferons (IFNs), which not only depleted anaerobic bacteria but also increased susceptibility to secondary Salmonella colitis.

“The increase in Proteobacteria appears to be mediated by type I interferons (IFNs) (18), which not only depleted anaerobic bacteria but also increased susceptibility to secondary Salmonella colitis.”

• cites [18] Domínguez-Cherit, 2009, Critically Ill patients with 2009 influenza A(H1N1) in Mexico, JAMA sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Antibiotic treatment prior to influenza infection ameliorated the degree of intestinal injury, but not lung injury, suggesting that gut dysbiosis contributed to local but not systemic inflammation.

“antibiotic treatment prior to influenza infection ameliorated the degree of intestinal injury, but not lung injury, suggesting that gut dysbiosis contributed to local but not systemic inflammation”

• cites [43] Wang, 2014, Respiratory influenza virus infection induces intestinal immune injury via microbiota-mediated Th17 cell-dependent inflammation, J Exp Med sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

Dysbiosis is associated with a variety of chronic diseases, many of which are characterized by chronic inflammation or abnormal metabolism, including inflammatory bowel disease, cardiovascular disease, and diabetes.

“Dysbiosis, or an imbalance in the normal composition of the microbiome, is associated with a variety of chronic diseases, many of which are characterized by chronic inflammation or abnormal metabolism, including inflammatory bowel disease, cardiovascular disease, and diabetes.”

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Caloric restriction also results in increased relative abundance of Proteobacteria and increased Bacteroidetes to Firmicutes ratio, raising the possibility that decreased oral intake during influenza may contribute to changes in the microbiome.

“caloric restriction also results in increased relative abundance of Proteobacteria and increased Bacteroidetes to Firmicutes ratio, raising the possibility that decreased oral intake during influenza may contribute to changes in the microbiome”

• cites [45] Bartley, 2017, Impact of age, caloric restriction, and influenza infection on mouse gut microbiome: an exploratory study of the role of age-related microbiome changes on influenza responses, Front Immunol sourceNot checked yet

  Not checked in the free run.

• cites [47] Groves, 2018, Respiratory disease following viral lung infection alters the murine gut microbiota, Front Immunol sourceNot checked yet

  Not checked in the free run.

• cites [49] Ley, 2006, Microbial ecology: human gut microbes associated with obesity, Nature sourceNot checked yet

  Not checked in the free run.

• cites [50] Ruiz, 2017, One-year calorie restriction impacts gut microbial composition but not its metabolic performance in obese adolescents, Environ Microbiol sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Macrophages from animals treated with antibiotics exhibited defective responses to type I and II IFNs and impaired capacity to limit viral replication, suggesting that intestinal microbiota provide immune stimulation that establishes an "activation threshold" for innate antiviral immune responses.

“Macrophages from animals treated with antibiotics exhibited defective responses to type I and II IFNs and impaired capacity to limit viral replication, suggesting that intestinal microbiota provide immune stimulation that establishes an “activation threshold” for innate antiviral immune responses”

• cites [52] Abt, 2012, Commensal bacteria calibrate the activation threshold of innate antiviral immunity, Immunity sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Mice given a 4 week oral course of broad-spectrum antibiotics before respiratory viral infection mounted an attenuated anti-PR8 antibody response, were incapable of inducing CD4+ T cell-mediated IFN-γ response to PR8 antigen, and had fewer influenza-specific CD8+ T cells.

“Mice given a 4 week oral course of broad-spectrum antibiotics before respiratory viral infection mounted an attenuated anti-PR8 antibody response, were incapable of inducing CD4+ T cell-mediated IFN-γ response to PR8 antigen, and had fewer influenza-specific CD8+T cells”

• cites [51] Ichinohe, 2011, Microbiota regulates immune defense against respiratory tract influenza A virus infection, Proc Natl Acad Sci USA sourceNot checked yet

  Not checked in the free run.

• cites [52] Abt, 2012, Commensal bacteria calibrate the activation threshold of innate antiviral immunity, Immunity sourceNot checked yet

  Not checked in the free run.

May combine two claims.

In a murine model of influenza infection, although total numbers of bacteria in the gut did not decrease, there was a reduction in quantities of segmented filamentous bacteria (SFB) and Lactobacillus/Lactococcus, accompanied by increases in Enterobacteriaceae.

“In a murine model of influenza infection, the investigators found that although the total numbers of bacteria in the gut did not decrease, there was a reduction in the quantities of segmented filamentous bacteria (SFB) and Lactobacillus/Lactococcus, accompanied by increases in Enterobacteriaceae.”

• cites [43] Wang, 2014, Respiratory influenza virus infection induces intestinal immune injury via microbiota-mediated Th17 cell-dependent inflammation, J Exp Med sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S4 (based).

Short-term perturbations in the gut microenvironment caused by illness, antibiotic usage, or dietary changes can alter the gut microbiome and subsequently lead to transient alterations in immune responses.

“Short-term perturbations in the gut microenvironment caused by illness, antibiotic usage, or dietary changes (e.g., starvation) can alter the gut microbiome and subsequently lead to transient alterations in immune responses.”

May combine two claims.

Germ-free mice and antibiotic-treated mice exhibit impaired antibody responses to seasonal influenza vaccination, which was restored by oral administration of flagellated E. coli, demonstrating a dependence on TLR5-mediated sensing of the host microbiota.

“Germ-free mice and antibiotic-treated mice also exhibit impaired antibody responses to seasonal influenza vaccination, which was restored by oral administration of flagellated E. coli, demonstrating a dependence on TLR5-mediated sensing of the host microbiota”

• cites [53] Oh, 2014, TLR5-mediated sensing of gut microbiota is necessary for antibody responses to seasonal influenza vaccination, Immunity sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

The respiratory tract is the main site of continuous contact with exogenous microbes.

“The respiratory tract is the main site of continuous contact with exogenous microbes.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Skin and oral cavity lineages are represented in the nasopharynx-e.g., Streptococcus, Staphylococcus, Corynebacterium, and Prevotella.

“Skin and oral cavity lineages are represented in the nasopharynx—e.g., Streptococcus, Staphylococcus, Corynebacterium, and Prevotella”

• cites [70] Charlson, 2011, Topographical continuity of bacterial populations in the healthy human respiratory tract, Am J Respir Crit Care Med sourceNot checked yet

  Not checked in the free run.

• cites [72] Ling, 2013, Pyrosequencing analysis of the human microbiota of healthy Chinese undergraduates, BMC Genomics sourceNot checked yet

  Not checked in the free run.

• cites [73] Allen, 2014, Characterization of the nasopharyngeal microbiota in health and during rhinovirus challenge, Microbiome sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Oral administration of a probiotic cocktail containing Lactobacillus restored the immune response and enhanced the activation of signaling pathways associated with recognition of single-stranded RNA virus.

“Oral administration of a probiotic cocktail containing Lactobacillus restored the immune response and enhanced the activation of signaling pathways associated with recognition of single-stranded RNA virus”

• cites [62] Wu, 2013, Microbiota regulates the TLR7 signaling pathway against respiratory tract influenza A virus infection, Curr Microbiol sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Clinical studies have shown that although probiotics do not influence the incidence of respiratory tract infection, they do reduce the severity of symptoms and duration of the illness.

“clinical studies have shown that although probiotics do not influence the incidence of respiratory tract infection, they do reduce the severity of symptoms and duration of the illness”

• cites [57] de, 2006, Probiotic bacteria reduced duration and severity but not the incidence of common cold episodes in a double blind, randomized, controlled trial, Vaccine sourceNot checked yet

  Not checked in the free run.

• cites [58] Vouloumanou, 2009, Probiotics for the prevention of respiratory tract infections: a systematic review, Int J Antimicrob Agents sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Antibiotic-pretreated animals displayed altered cytokine profiles in the lung compared to untreated controls following S. pneumoniae infection, including significantly decreased TNF-α levels at 6 and 24 h after infection.

“Antibiotic-pretreated animals displayed altered cytokine profiles in the lung compared to untreated controls following S. pneumoniae infection, including significantly decreased TNF-α levels at 6 and 24 h after infection.”

• cites [55] Schuijt, 2016, The gut microbiota plays a protective role in the host defence against pneumococcal pneumonia, Gut sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Animals fed a high fiber diet had increased generation of SCFAs, leading to enhanced antiviral CD8+ T cell immune responses and attenuated neutrophil-mediated lung injury during influenza infection, resulting in improved survival.

“animals fed a high fiber diet had increased generation of SCFAs, leading to enhanced antiviral CD8+ T cell immune responses and attenuated neutrophil-mediated lung injury during influenza infection, resulting in improved survival”

• cites [63] Trompette, 2018, Dietary fiber confers protection against flu by shaping Ly6c- patrolling monocyte hematopoiesis and CD8+ T cell metabolism, Immunity sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing).

The oropharynx contains members of Firmicutes, Proteobacteria, and Bacteroidetes, including Streptococcus, Neisseria, Haemophilus, and Lachnospira spp.

“The oropharynx contains members of Firmicutes, Proteobacteria, and Bacteroidetes, including Streptococcus, Neisseria, Haemophilus, and Lachnospira spp.”

• cites [68] Lemon, 2010, Comparative analyses of the bacterial microbiota of the human nostril and oropharynx, MBio sourceNot checked yet

  Not checked in the free run.

• cites [70] Charlson, 2011, Topographical continuity of bacterial populations in the healthy human respiratory tract, Am J Respir Crit Care Med sourceNot checked yet

  Not checked in the free run.

• cites [71] Yi, 2014, Profiling bacterial community in upper respiratory tracts, BMC Infect Dis sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing).

In healthy adults, bacteria present in the nasal cavity are typically those associated with skin, predominantly members of the Actinobacteria, followed by Firmicutes, and Proteobacteria.

“In healthy adults, bacteria present in the nasal cavity are typically those associated with skin, predominantly members of the Actinobacteria (e.g., Corynebacterium spp., Propionibacterium spp.), followed by Firmicutes (e.g., Staphylococcus spp.), and Proteobacteria”

• cites [67] Frank, 2010, The human nasal microbiota and Staphylococcus aureus carriage, PLoS ONE sourceNot checked yet

  Not checked in the free run.

• cites [68] Lemon, 2010, Comparative analyses of the bacterial microbiota of the human nostril and oropharynx, MBio sourceNot checked yet

  Not checked in the free run.

• cites [69] Bassis, 2014, The nasal cavity microbiota of healthy adults, Microbiome sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Oral administration of Lactobacillus plantarum enhanced the type I IFN response and lowered viral titers in the lungs in a murine model of influenza infection.

“oral administration of Lactobacillus plantarum enhanced the type I IFN response and lowered viral titers in the lungs in a murine model of influenza infection”

• cites [60] Maeda, 2009, Oral administration of heat-killed Lactobacillus plantarum L-137 enhances protection against influenza virus infection by stimulation of type I interferon production in mice, Int Immunopharmacol sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Antibiotic-treated mice exhibited markedly decreased fecal and serum DAT levels, which was associated with attenuated type I IFN responses to influenza infection and increased mortality.

“Antibiotic-treated mice exhibited markedly decreased fecal and serum DAT levels, which was associated with attenuated type I IFN responses to influenza infection and increased mortality”

• cites [59] Steed, 2017, The microbial metabolite desaminotyrosine protects from influenza through type I interferon, Science sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Microbiome depletion led to decreased survival, increased lung bacterial burden, and increased systemic dissemination of bacteria in mice challenged with S. pneumoniae.

“microbiome depletion led to decreased survival, increased lung bacterial burden, and increased systemic dissemination of bacteria”

• cites [55] Schuijt, 2016, The gut microbiota plays a protective role in the host defence against pneumococcal pneumonia, Gut sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

Several factors are known to influence airway microbiome composition including infection history, age, genetics, and structural lung disease.

“Several factors are known to influence airway microbiome composition including infection history, age, genetics, and structural lung disease.”

May combine two claims.

SFB-deficient animals have increased lung bacterial burdens and more severe pneumonia when challenged with MRSA, which was associated with decreased IL-17-mediated responses in the lung.

“SFB-deficient animals have increased lung bacterial burdens and more severe pneumonia when challenged with methicillin-resistant Staphylococcus aureus (MRSA) (54), which was associated with decreased IL-17-mediated responses in the lung.”

• cites [54] Gauguet, 2015, Intestinal Microbiota of Mice Influences Resistance to Staphylococcus aureus Pneumonia, Infect Immun sourceNot checked yet

  Not checked in the free run.

May combine two claims.

In the microbiota-depleted group, alveolar macrophages and blood neutrophils exhibited decreased phagocytic activity, and decreased inflammatory cytokine production following ex vivo stimulation by TLR ligands such as LTA.

“in the microbiota-depleted group, alveolar macrophages and blood neutrophils exhibited decreased phagocytic activity, and decreased inflammatory cytokine production following ex vivo stimulation by Toll-like receptor (TLR) ligands such as lipoteichoic acid (LTA)”

• cites [55] Schuijt, 2016, The gut microbiota plays a protective role in the host defence against pneumococcal pneumonia, Gut sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based). May combine two claims.

The URT and LRT have similar microbial community compositions, although microbe densities are much higher in the former in healthy hosts.

“The URT and LRT have similar microbial community compositions, although microbe densities are much higher in the former in healthy hosts.”

May combine two claims.

Individuals with chronic airway diseases (e.g., cystic fibrosis, COPD) have increased bacterial populations in the lungs and differences in the relative abundance of certain species.

“Individuals with chronic airway diseases (e.g., cystic fibrosis, COPD) have increased bacterial populations in the lungs (77) and differences in the relative abundance of certain species”

• cites [77] Venkataraman, 2015, Application of a neutral community model to assess structuring of the human lung microbiome, MBio sourceNot checked yet

  Not checked in the free run.

• cites [81] Rogers, 2015, Respiratory microbiota: addressing clinical questions, informing clinical practice, Thorax sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

The major phyla in healthy lungs are Bacteroidetes and Firmicutes, which mainly include Prevotella, Veillonella, and Streptococcus.

“The major phyla in healthy lungs are Bacteroidetes and Firmicutes, which mainly include Prevotella, Veillonella, and Streptococcus”

• cites [78] Morris, 2013, Comparison of the respiratory microbiome in healthy nonsmokers and smokers, Am J Respir Crit Care Med sourceNot checked yet

  Not checked in the free run.

• cites [79] Segal, 2013, Enrichment of lung microbiome with supraglottic taxa is associated with increased pulmonary inflammation, Microbiome sourceNot checked yet

  Not checked in the free run.

• cites [80] Dickson, 2015, Spatial variation in the healthy human lung microbiome and the adapted island model of lung biogeography, Ann Am Thorac Soc sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Contrary to dogma that normal healthy lungs are a sterile environment, a distinct, and somewhat dynamic lung microbiome can be identified using sequencing technology, with microaspiration serving as the primary route of microbial immigration from the URT to the LRT.

“Contrary to dogma that normal healthy lungs are a sterile environment, a distinct, and somewhat dynamic lung microbiome can be identified using sequencing technology, with microaspiration serving as the primary route of microbial immigration from the URT to the LRT”

• cites [76] Bassis, 2015, Analysis of the upper respiratory tract microbiotas as the source of the lung and gastric microbiotas in healthy individuals, MBio sourceNot checked yet

  Not checked in the free run.

• cites [77] Venkataraman, 2015, Application of a neutral community model to assess structuring of the human lung microbiome, MBio sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

A limited number of pathogens including Streptococcus pneumoniae, Neisseria meningitides, and Haemophilus influenzae are commensal bacteria of the URT.

“A limited number of pathogens including Streptococcus pneumoniae, Neisseria meningitides, and Haemophilus influenzae are commensal bacteria of the URT.”

May combine two claims.

Both studies included subjects ranging from infants to adults >80 years of age, limiting conclusions about age-related effects.

“Both studies included subjects ranging from infants to adults >80 years of age, limiting conclusions about age-related effects.”

• cites [71] Yi, 2014, Profiling bacterial community in upper respiratory tracts, BMC Infect Dis sourceNot checked yet

  Not checked in the free run.

• cites [100] Edouard, 2018, The nasopharyngeal microbiota in patients with viral respiratory tract infections is enriched in bacterial pathogens, Eur J Clin Microbiol Infect Dis sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Unlike other diseases where decreased diversity is considered deleterious to the host, the effects of viral infections on diversity per se are variable and not presently considered a good indicator of risk for complications, including secondary bacterial pneumonias.

“Thus, unlike other diseases where decreased diversity is considered deleterious to the host, the effects of viral infections on diversity per se are variable and not presently considered a good indicator of risk for complications, including secondary bacterial pneumonias.”

May combine two claims.

Children with severe influenza showed decreased relative abundance of S. aureus and increased abundance of Prevotella, Streptobacillus, Porphyromonas, Granulicatella, Veillonella, Fusobacterium, and Haemophilus.

“Children with severe influenza showed decreased relative abundance of S. aureus and increased abundance of Prevotella, Streptobacillus, Porphyromonas, Granulicatella, Veillonella, Fusobacterium, and Haemophilus.”

• cites [105] Langevin, 2017, Early nasopharyngeal microbial signature associated with severe influenza in children: a retrospective pilot study, J Gen Virol sourceNot checked yet

  Not checked in the free run.

May combine two claims.

RSV-infected mice who underwent antibiotic-mediated depletion of Streptococcus viridans in the nasopharynx exhibited increases in number of inflammatory lymphocytes and airway hyperresponsiveness, and decreases in regulatory T cell number and transforming growth factor-β production.

“RSV-infected mice who underwent antibiotic-mediated depletion of Streptococcus viridans in the nasopharynx exhibited increases in number of inflammatory lymphocytes and airway hyperresponsiveness, and decreases in regulatory T cell number and transforming growth factor-β production”

• cites [103] Ni, 2012, Pharyngeal microflora disruption by antibiotics promotes airway hyperresponsiveness after respiratory syncytial virus infection, PLoS ONE sourceNot checked yet

  Not checked in the free run.

May combine two claims.

In a study of mice colonized with S. pneumoniae and then infected with influenza A virus 3 days after, S. pneumoniae transmission occurred only when all mice were infected with influenza and was blocked by an influenza-neutralizing antibody.

“In a study of mice colonized with S. pneumoniae and then infected with influenza A virus 3 days after, S. pneumoniae transmission occurred only when all mice were infected with influenza and was blocked by an influenza-neutralizing antibody”

• cites [95] Diavatopoulos, 2010, Influenza A virus facilitates Streptococcus pneumoniae transmission and disease, FASEB J sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

In healthy children, the major phyla among nasopharyngeal microbiotas are Proteobacteria, Firmicutes, Bacteroidetes, Actinobacteria, and Fusobacteria, with Moraxella, Haemophilus, Streptococcus, Flavobacteria, Dolosigranulum, Corynebacterium, and Neisseria as predominant genera.

“In healthy children, the major phyla among nasopharyngeal microbiotas are Proteobacteria, Firmicutes, Bacteroidetes, Actinobacteria, and Fusobacteria, with Moraxella, Haemophilus, Streptococcus, Flavobacteria, Dolosigranulum, Corynebacterium, and Neisseria as predominant genera.”

• cites [114] Bogaert, 2011, Variability and diversity of nasopharyngeal microbiota in children: a metagenomic analysis, PLoS ONE sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Another complicating factor particularly in cross-sectional studies examining the microbiome during viral infections is that the groups are not well-controlled and the sample numbers are relatively small considering the number of variables that could affect the respiratory tract microbiome.

“Another complicating factor particularly in cross-sectional studies examining the microbiome during viral infections is that the groups are not well-controlled and the sample numbers are relatively small considering the number of variables that could affect the respiratory tract microbiome–such as age, gender, oral hygiene and nose-picking habits, healthcare-based employment status, smoking status”

May combine two claims.

Mean relative abundances of Haemophilus, Moraxella, Staphylococcus, and Corynebacterium varied significantly between summer and fall samples and between age groups.

“although mean relative abundances of Haemophilus, Moraxella, Staphylococcus, and Corynebacterium varied significantly between summer and fall samples and between age groups.”

• cites [115] Pérez-Losada, 2017, Nasopharyngeal microbiome diversity changes over time in children with asthma, PLoS ONE sourceNot checked yet

  Not checked in the free run.

May combine two claims.

The underlying type of viral infection, sampling timepoint after onset of infection, severity of infection, and concomitant antimicrobial usage are confounding factors.

“The underlying type of viral infection, sampling timepoint after onset of infection, severity of infection, and concomittant antimicrobial usage are other confounding factors.”

May combine two claims.

These studies demonstrated that there was considerable inter-subject variability, highlighting the need for longitudinal studies to decipher changes following viral infection.

“However, these studies demonstrated that there was considerable inter-subject variability, highlighting the need for longitudinal studies to decipher changes following viral infection.”

• cites [108] Leung, 2013, Modulation of potential respiratory pathogens by pH1N1 viral infection, Clin Microbiol Infect sourceNot checked yet

  Not checked in the free run.

• cites [109] Chaban, 2013, Characterization of the upper respiratory tract microbiomes of patients with pandemic H1N1 influenza, PLoS ONE sourceNot checked yet

  Not checked in the free run.

• cites [110] Greninger, 2010, A metagenomic analysis of pandemic influenza A (2009 H1N1) infection in patients from North America, PLoS ONE sourceNot checked yet

  Not checked in the free run.

May combine two claims.

An investigation of the frequency and seasonal variation in bacterial and viral load in asymptomatic healthcare professionals during the winter and summer months showed that of the 100 subjects tested during the winter, 34 were colonized with at least one bacterial species and 11 tested positive for at least one virus.

“An investigation of the frequency and seasonal variation in bacterial and viral load in asymptomatic healthcare professionals during the winter and summer months showed that of the 100 subjects tested during the winter, 34 were colonized with at least one bacterial species and 11 tested positive for at least one virus.”

• cites [116] Hassoun, 2015, Seasonal variation of respiratory pathogen colonization in asymptomatic health care professionals: A single-center, cross-sectional, 2-season observational study, Am J Infect Control sourceNot checked yet

  Not checked in the free run.

May combine two claims.

In the nasopharyngeal compartment of Aboriginal and non-Aboriginal children in Australia, positive associations were detected between hRV and S. pneumoniae, H. influenza, and Moraxella catarrhalis carriage as well as between adenovirus and M. catarrhalis.

“In the nasopharyngeal compartment of Aboriginal and non-Aboriginal children in Australia, positive associations were detected between hRV and S. pneumoniae, H. influenza, and Moraxella catarrhalis carriage as well as between adenovirus and M. catarrhalis (111).”

• cites [111] Jacoby, 2007, Kalgoorlie Otitis Media Research Project Team. Modelling the co-occurrence of Streptococcus pneumoniae with other bacterial and viral pathogens in the upper respiratory tract, Vaccine sourceNot checked yet

  Not checked in the free run.

May combine two claims.

These profiles were not associated with virus type but were linked to the age of subjects.

“These profiles, however, were not associated with virus type but were linked to the age of subjects (71).”

• cites [71] Yi, 2014, Profiling bacterial community in upper respiratory tracts, BMC Infect Dis sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Changes in nasopharyngeal microbiome diversity were observed across seasons, with a predominance of Proteobacteria and Fusobacteria in fall-winter and Bacteroidetes and Firmicutes in spring; these differences were independent of recent antibiotics and viral co-infection.

“Changes in nasopharyngeal microbiome diversity were observed across seasons, with a predominance of Proteobacteria and Fusobacteria in fall-winter and Bacteroidetes and Firmicutes in spring; these differences were independent of recent antibiotics and viral co-infection (114).”

• cites [114] Bogaert, 2011, Variability and diversity of nasopharyngeal microbiota in children: a metagenomic analysis, PLoS ONE sourceNot checked yet

  Not checked in the free run.

May combine two claims.

In a mouse model, bacterial density in the nasopharynx after LAIV administration was increased as much as 100,000 times compared to influenza-naive hosts, and the duration of carriage of S. pneumoniae or S. aureus was also increased 2 to 5-fold.

“In a mouse model, bacterial density in the nasopharynx after LAIV administration was increased as much as 100,000 times compared to influenza-naive hosts, and the duration of carriage of S. pneumoniae or S. aureus was also increased 2 to 5-fold (121).”

• cites [121] Mina, 2014, Live attenuated influenza vaccine enhances colonization of Streptococcus pneumoniae and Staphylococcus aureus in mice, MBio sourceNot checked yet

  Not checked in the free run.

May combine two claims.

In healthy adult volunteers, intranasal LAIV administration induced an increase in the diversity of the nasopharyngeal microbiome, as well as relative abundances of Staphylococcus and Bacteroides.

“In healthy adult volunteers, it was demonstrated that intranasal LAIV administration induced an increase in the diversity of the nasopharyngeal microbiome, as well as relative abundances of Staphylococcus and Bacteroides (107).”

• cites [107] Tarabichi, 2015, The administration of intranasal live attenuated influenza vaccine induces changes in the nasal microbiota and nasal epithelium gene expression profiles, Microbiome sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Nasopharyngeal sampling showed decreased relative abundance of Haemophilus and Neisseria spp., but an increase in the normal nasal commensal, Propionibacterium, in subjects following hRV infection.

“Nasopharyngeal sampling showed completely opposite results, with decreased relative abundance of Haemophilus and Neisseria spp., but an increase in the normal nasal commensal, Propionibacterium, in subjects following hRV infection (73).”

• cites [73] Allen, 2014, Characterization of the nasopharyngeal microbiota in health and during rhinovirus challenge, Microbiome sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Administration of live attenuated influenza vaccine (LAIV), which is nasally instilled, to healthy children increased the nasal colonization density of S. pneumoniae in subjects who harbored this bacterium at the time of vaccination, and transiently increased rates of colonization by H. influenza.

“Administration of live attenuated influenza vaccine (LAIV), which is nasally instilled, to healthy children increased the nasal colonization density of S. pneumoniae in subjects who harbored this bacterium at the time of vaccination, and transiently increased rates of colonization by H. influenza (120).”

• cites [120] Thors, 2016, The effects of live attenuated influenza vaccine on nasopharyngeal bacteria in healthy 2 to 4 year olds. a randomized controlled trial, Am J Respir Crit Care Med sourceNot checked yet

  Not checked in the free run.

May combine two claims.

In contrast, of the 100 subjects tested during the summer, 37 harbored at least one bacterium (mainly MRSA and K. pneumoniae) and four tested positive for one virus.

“In contrast, of the 100 subjects tested during the summer, 37 harbored at least one bacterium (mainly MRSA and K. pneumoniae) and four tested positive for one virus (116).”

• cites [116] Hassoun, 2015, Seasonal variation of respiratory pathogen colonization in asymptomatic health care professionals: A single-center, cross-sectional, 2-season observational study, Am J Infect Control sourceNot checked yet

  Not checked in the free run.

May combine two claims.

In the oropharyngeal compartment, rhinovirus infection was associated with a strong trend toward transient increases in the relative abundances of H. parainfluenzae, Neisseria subflava and a weak trend toward an increase in S. aureus.

“In the oropharyngeal compartment, rhinovirus infection was associated with a strong trend toward transient increases in the relative abundances of H. parainfluenzae, Neisseria subflava and a weak trend toward an increase in S. aureus (119).”

• cites [119] Hofstra, 2015, Changes in microbiota during experimental human Rhinovirus infection, BMC Infect Dis sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Another study of 31 families with small children using longitudinal nasal swab sampling demonstrated that rhinovirus infection was associated with increased acquisition of S. pneumoniae from the community as well as increased transmission of S. pneumoniae within the family.

“Another study of 31 families with small children using longitudinal nasal swab sampling demonstrated that rhinovirus infection was associated with increased acquisition of S. pneumoniae from the community as well as increased transmission of S. pneumoniae within the family (118).”

• cites [118] Karppinen, 2017, Acquisition and transmission of streptococcus pneumoniae are facilitated during rhinovirus infection in families with children, Am J Respir Crit Care Med sourceNot checked yet

  Not checked in the free run.

May combine two claims.

The percentage of colonized children and bacterial density were also higher at asymptomatic visits in which virus was detected than at those in which virus was not detected.

“Interestingly, the percentage of colonized children and bacterial density were also higher at asymptomatic visits in which virus was detected than at those in which virus was not detected (117).”

• cites [117] DeMuri, 2018, Dynamics of bacterial colonization with streptococcus pneumoniae, haemophilus influenzae, and moraxella catarrhalis during symptomatic and asymptomatic viral upper respiratory tract infection, Clin Infect Dis sourceNot checked yet

  Not checked in the free run.

May combine two claims.

In subjects with chronic obstructive pulmonary disease (COPD) after hRV infection but not in healthy individuals, there was an increase in bacterial burden and growth of bacteria present at baseline, particularly H. influenzae.

“In subjects with chronic obstructive pulmonary disease (COPD) after hRV infection but not in healthy individuals, there was an increase in bacterial burden and growth of bacteria present at baseline, particularly H. influenzae (124).”

• cites [124] Molyneaux, 2013, Outgrowth of the bacterial airway microbiome after rhinovirus exacerbation of chronic obstructive pulmonary disease, Am J Respir Crit Care Med sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Mucus production in the respiratory tract is increased to facilitate viral clearance during infections, but excessive mucus production can lead to airway obstruction by impeding mucociliary clearance.

“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).”

• cites [125] Vareille, 2011, The airway epithelium: soldier in the fight against respiratory viruses, Clin Microbiol Rev sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Increased upper respiratory tract persistence of S. aureus as well as increased risk of S. aureus pneumonia was observed in flu-infected wildtype mice compared to mice lacking the type III IFN receptor.

“Increased upper respiratory tract persistence of S. aureus as well as increased risk of S. aureus pneumonia was observed in flu-infected wildtype mice compared to mice lacking the type III IFN receptor (123).”

• cites [123] Planet, 2016, Lambda interferon restructures the nasal microbiome and increases susceptibility to staphylococcus aureus superinfection, MBio sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Respiratory viruses not only alter the bacterial community in the URT, but also promote bacterial colonization of the LRT by a variety of mechanisms that impair bacterial clearance.

“Respiratory viruses not only alter the bacterial community in the URT, but also promote bacterial colonization of the LRT by a variety of mechanisms that impair bacterial clearance.”

Probably not a substantial claim: may not pass S3 (load-bearing).

Compared to studies of the URT microbiome, studies of the LRT microbiome following viral infections are relatively scarce due to the difficulty of obtaining uncontaminated samples from the lung.

“Compared to studies of the URT microbiome, studies of the LRT microbiome following viral infections are relatively scarce due to the difficulty of obtaining uncontaminated samples from the lung.”

May combine two claims.

Viral infections can reduce ciliary beat frequency and the number of ciliated cells, disrupt the coordinated movement of cilia, and impede the repair of respiratory epithelial cells, further leading to reduced mucociliary clearance.

“Second, viral infections can also reduce ciliary beat frequency and the number of ciliated cells, disrupt the coordinated movement of cilia, and impede the repair of respiratory epithelial cells, further leading to reduced mucociliary clearance (126, 127).”

• cites [126] Pittet, 2010, Influenza virus infection decreases tracheal mucociliary velocity and clearance of Streptococcus pneumoniae, Am J Respir Cell Mol Biol sourceNot checked yet

  Not checked in the free run.

• cites [127] Smith, 2014, Ciliary dyskinesia is an early feature of respiratory syncytial virus infection, Eur Respir J sourceNot checked yet

  Not checked in the free run.

Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

Samples of convenience, such as sputum, suffer from oral contamination, but bronchoscopic samples are invasive and expensive to obtain on a regular basis.

“Samples of convenience, such as sputum, suffer from oral contamination, but bronchoscopic samples are invasive and expensive to obtain on a regular basis.”

May combine two claims.

C. pseudodiphtheriticum inhibited S. aureus growth, whereas C. accolens and S. aureus appeared to support each other's growth.

“Subsequent studies by another group reported that C. pseudodiphtheriticum inhibited S. aureus growth, whereas C. accolens and S. aureus appeared to support each other's growth (139).”

• cites [139] Yan, 2013, Nasal microenvironments and interspecific interactions influence nasal microbiota complexity and S. aureus carriage, Cell Host Microbe sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Influenza infection perturbs the respiratory microbiome, leading to the production of secondary metabolites including immune-modulating molecules.

“These data imply that influenza infection perturbs the respiratory microbiome, leading to the production of secondary metabolites including immune-modulating molecules.”

• cites [108] Leung, 2013, Modulation of potential respiratory pathogens by pH1N1 viral infection, Clin Microbiol Infect sourceNot checked yet

  Not checked in the free run.

May combine two claims.

A recent preclinical study using a murine model of RSV and S. pneumoniae superinfection employed nasal priming by a C. pseudodiphtheriticum strain to augment host defense against the viral infection, which enhanced clearance of secondary bacterial challenge and reduced lung injury measures.

“Interestingly, a recent preclinical study using a murine model of RSV and S. pneumoniae superinfection employed nasal priming by a C. pseudodiphtheriticum strain to augment host defense against the viral infection, which enhanced clearance of secondary bacterial challenge and reduced lung injury measures (140).”

• cites [140] Kanmani, 2017, Respiratory commensal bacteria corynebacterium pseudodiphtheriticum improves resistance of infant mice to respiratory syncytial virus and streptococcus pneumoniae superinfection, Front Microbiol sourceNot checked yet

  Not checked in the free run.

May combine two claims.

Corynebacterium spp. were enriched in children who were not nasally colonized with pneumococcus, and C. accolens inhibit S. pneumoniae growth in vitro by expressing a lipase that releases free fatty acids from skin surface triacylglycerols, which inhibit pneumococcal growth.

“Conversely, other investigators observed that Corynebacterium spp. were enriched in children who were not nasally colonized with pneumococcus, and demonstrated that C. accolens inhibit S. pneumoniae growth in vitro by expressing a lipase that releases free fatty acids from skin surface triacylglycerols, which inhibit pneumococcal growth.”

Probably not a substantial claim: may not pass S3 (load-bearing).

The mechanism of eradication appeared to be bacteriocin-independent.

“The mechanism appeared to be bacteriocin-independent.”

• cites [137] Uehara, 2000, Bacterial interference among nasal inhabitants: eradication of Staphylococcus aureus from nasal cavities by artificial implantation of Corynebacterium sp, J Hosp Infect sourceNot checked yet

  Not checked in the free run.

Classified as probably not a substantial claim.

It is possible that the immune response incited by acute viral infections, changes in the host epithelial surface caused by the virus, or the virus itself might lead to elimination of a host commensal that is responsible for keeping pathobionts in check.

“Thus, it is possible that the immune response incited by acute viral infections, changes in the host epithelial surface caused by the virus, or the virus itself might lead to elimination of a host commensal that is responsible for keeping pathobionts in check.”

• AssumptionRests on an assumption: Interspecies competition maintains homeostasis of the microbial community, preventing one microbe from dominating the community.

May combine two claims.

Viruses impair bacterial biofilm formation and disrupt existing biofilm.

“Viruses have also been found to impair bacterial biofilm formation and disrupt existing biofilm (141–144).”

• cites [141] Reddinger, 2016, Host physiologic changes induced by influenza a virus lead to staphylococcus aureus biofilm dispersion and transition from asymptomatic colonization to invasive disease, MBio sourceNot checked yet

  Not checked in the free run.

• cites [142] Pettigrew, 2014, Dynamic changes in the Streptococcus pneumoniae transcriptome during transition from biofilm formation to invasive disease upon influenza A virus infection, Infect Immun sourceNot checked yet

  Not checked in the free run.

• cites [143] Marks, 2013, Interkingdom signaling induces Streptococcus pneumoniae biofilm dispersion and transition from asymptomatic colonization to disease, MBio sourceNot checked yet

  Not checked in the free run.

• cites [144] Reddinger, 2018, Streptococcus pneumoniae modulates staphylococcus aureus biofilm dispersion and the transition from colonization to invasive disease, MBio sourceNot checked yet

  Not checked in the free run.