Viral and bacterial co-infection in severe pneumonia triggers innate immune responses and specifically enhances IP-10: a translational study.
Open accessAbstract
Mixed viral and bacterial infections are widely described in community-acquired pneumonia; however, the clinical implications of co-infection on the associated immunopathology remain poorly studied. In this study, microRNA, mRNA and cytokine/chemokine secretion profiling were investigated for human monocyte-derived macrophages infected in-vitro with Influenza virus A/H1N1 and/or Streptococcus pneumoniae. We observed that the in-vitro co-infection synergistically increased interferon-γ-induced protein-10 (CXCL10, IP-10) expression compared to the singly-infected cells conditions. We demonstrated that endogenous miRNA-200a-3p, whose expression was synergistically induced following co-infection, indirectly regulates CXCL10 expression by targeting suppressor of cytokine signaling-6 (SOCS-6), a well-known regulator of the JAK-STAT signaling pathway. Additionally, in a subsequent clinical pilot study, immunomodulators levels were evaluated in samples from 74 children (≤5 years-old) hospitalized with viral and/or bacterial community-acquired pneumonia. Clinically, among the 74 cases of pneumonia, patients with identified mixed-detection had significantly higher (3.6-fold) serum IP-10 levels than those with a single detection (P = 0.03), and were significantly associated with severe pneumonia (P < 0.01). This study demonstrates that viral and bacterial co-infection modulates the JAK-STAT signaling pathway and leads to exacerbated IP-10 expression, which could play a major role in the pathogenesis of pneumonia.
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Co-infection results in a synergistic increase in type II IFN (IFNγ) compared to individual infection of influenza or S. pneumoniae.
“Co-infection also results in a synergistic increase in type II IFN (IFNγ) when compared to individual infection of influenza or S. pneumoniae”
From Secondary bacterial infections associated with influenza pandemics (2017) · cites this paper as Hoffmann et al., 2016
IP-10 attracts various immune cells including activated T cells, monocytes and macrophages, causing inflammation.
“IP-10 attracts various immune cells including activated T cells, monocytes and macrophages, therefore causing inflammation (Dufour et al., 2002; Hoffmann et al., 2016).”
From Secondary bacterial infections associated with influenza pandemics (2017) · cites this paper as Hoffmann et al., 2016
Patients suffering severe pneumonia show significantly higher levels of IP-10 than those with minor cases of pneumonia.
“Patients suffering severe pneumonia show significantly higher levels of IP-10 than those with minor cases of pneumonia.”
From Secondary bacterial infections associated with influenza pandemics (2017) · cites this paper as Hoffmann et al., 2016
CXCL10 (IP-10) is secreted in response to IFNγ.
“CXCL10 (aka IFNγ-induced protein 10/IP-10) is secreted in response.”
From Secondary bacterial infections associated with influenza pandemics (2017) · cites this paper as Hoffmann et al., 2016
Viral and bacterial co-infection of monocyte-derived macrophages synergistically induces a pro-inflammatory response related to type-I IFN and JAK-STAT signaling pathways.
“Viral and bacterial co-infection of monocyte derived macrophages synergistically induces a pro-inflammatory response related to the type-I IFN and JAK-STAT signaling pathways (Hoffmann et al., 2016).”
From Secondary bacterial infections associated with influenza pandemics (2017) · cites this paper as Hoffmann et al., 2016
IP-10 is increased during H. influenzae and S. aureus co-infection and correlates with pneumonia etiology.
“IP-10 is increased during H. influenzae and S. aureus co-infection as well, and like with S. pneumoniae, correlates with/highlights pneumonia etiology (Hoffmann et al., 2016).”
From Secondary bacterial infections associated with influenza pandemics (2017) · cites this paper as Hoffmann et al., 2016
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References 46 · Cited by 53
- Authors
- Hoffmann, J., Machado, D., Terrier, O., Pouzol, S., Messaoudi, M., Basualdo, W., Espínola, E. E., Guillen, R. M., Rosa-Calatrava, M., Picot, V., Bénet, T., Endtz, H., Russomando, G., & Paranhos-Baccalà, G.
- Affiliations
- Inserm (FR)
- Lyon 1 Université (FR)
- Ministerio de Salud Pública y Bienestar Social (PY)
- Universidad Nacional de Asunción (PY)
- Hospices Civils de Lyon (FR)
- ORCID
- Venue
- Scientific Reports
- Published
- 2016-12-06
- Volume
- 6
- Issue
- 1
- Pages
- 38532-38532
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5138590
- OpenAlex
- W2560840497
- Cited by
- 53
- References
- 46
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 2 · 2023: 3 · 2022: 7 · 2021: 7 · 2020: 3 · 2019: 8 · 2018: 12 · 2017: 3
- FWCI
- 7.19
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Funders
- Universidad Nacional de Asunción
- Fondation Mérieux
- Topics
- Health Sciences › Medicine › Epidemiology › Pneumonia and Respiratory Infections
- Health Sciences › Medicine › Epidemiology › Respiratory viral infections research
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Keywords
- viral-bacterial coinfection, community-acquired pneumonia, severe pneumonia, CXCL10, miR-200a-3p, JAK/STAT signaling, innate immune response, H1N1 influenza, Streptococcus pneumoniae, monocyte-derived macrophages, chemokines, children
- MeSH terms
- Adult, Aged, Bacterial Infections, Base Sequence, Female, Humans, Immunity, Innate, Infant, Macrophages, Male, Middle Aged, Models, Biological, Pneumonia, RNA, Messenger, Streptococcus pneumoniae, Virus Diseases, Gene Expression Profiling, MicroRNAs, Suppressor of Cytokine Signaling Proteins, Influenza A Virus, H1N1 Subtype, Chemokine CXCL10, Young Adult, Translational Research, Biomedical, Coinfection
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