Influenza A inhibits Th17-mediated host defense against bacterial pneumonia in mice.

Kudva, Anupa; Scheller, Erich V; Robinson, Keven M; Crowe, Chris R; Choi, Sun Mi; Slight, Samantha R; Khader, Shabaana A; Dubin, Patricia J; Enelow, Richard I; Kolls, Jay K; Alcorn, John F

doi:10.4049/jimmunol.1002194

Cited by 346Influenza Virus Research Studiesinterferon and immune responsesPsoriasis: Treatment and Pathogenesis

Influenza A inhibits Th17-mediated host defense against bacterial pneumonia in mice.

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Kudva, Anupa, Scheller, Erich V, Robinson, Keven M, Crowe, Chris R, Choi, Sun Mi, Slight, Samantha R, Khader, Shabaana A, Dubin, Patricia J +3 more·2011·The Journal of Immunology

DOI 10.4049/jimmunol.1002194PMC PMC4275066

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Abstract

Staphylococcus aureus is a significant cause of hospital and community acquired pneumonia and causes secondary infection after influenza A. Recently, patients with hyper-IgE syndrome, who often present with S. aureus infections of the lung and skin, were found to have mutations in STAT3, required for Th17 immunity, suggesting a potential critical role for Th17 cells in S. aureus pneumonia. Indeed, IL-17R(-/-) and IL-22(-/-) mice displayed impaired bacterial clearance of S. aureus compared with that of wild-type mice. Mice challenged with influenza A PR/8/34 H1N1 and subsequently with S. aureus had increased inflammation and decreased clearance of both virus and bacteria. Coinfection resulted in greater type I and II IFN production in the lung compared with that with virus infection alone. Importantly, influenza A coinfection resulted in substantially decreased IL-17, IL-22, and IL-23 production after S. aureus infection. The decrease in S. aureus-induced IL-17, IL-22, and IL-23 was independent of type II IFN but required type I IFN production in influenza A-infected mice. Furthermore, overexpression of IL-23 in influenza A, S. aureus-coinfected mice rescued the induction of IL-17 and IL-22 and markedly improved bacterial clearance. These data indicate a novel mechanism by which influenza A-induced type I IFNs inhibit Th17 immunity and increase susceptibility to secondary bacterial pneumonia.

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Type I IFN-mediated inhibition of Th17 immunity reduces CD4+ T cells and gamma delta T cells, leading to reduced production of IL-17 and IL-22 and preventing clearance of bacteria.
“and therefore there is a reduction in the levels of CD4+ T cells and gamma delta T cells and hence a reduction in the production of IL-17 and IL-22, preventing the clearance of bacteria (Shahangian et al., 2009; Kudva et al., 2011; Mulcahy and McLoughlin, 2016).”
From Secondary bacterial infections associated with influenza pandemics (2017) · cites this paper as Kudva et al., 2011
Type I IFNs inhibit IL-23-dependent induction of Th17 immunity.
“Additionally, Type I IFNs inhibit interleukin 23 (IL-23) dependent induction of T helper cell 17 (Th17) immunity”
From Secondary bacterial infections associated with influenza pandemics (2017) · cites this paper as Kudva et al., 2011

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Influenza A Exacerbates Staphylococcus aureus Pneumonia by Attenuating IL-1β Production in Mice
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Authors: Kudva, A., Scheller, E. V., Robinson, K. M., Crowe, C. R., Choi, S. M., Slight, S. R., Khader, S. A., Dubin, P. J., Enelow, R. I., Kolls, J. K., & Alcorn, J. F.
Affiliations: Children's Hospital of Pittsburgh (US)
Department of Pediatrics, Children’s Hospital of Pittsburgh, University of Pittsburgh Medical Center , Pittsburgh, PA 15224
Louisiana State University Health Sciences Center New Orleans (US)
Dartmouth College (US)
Corresponding author: Kudva, Anupa
ORCID: Robinson, Keven M
Choi, Sun Mi
Khader, Shabaana A
Enelow, Richard I
Kolls, Jay K
Alcorn, John F
Venue: The Journal of Immunology
Publisher: Oxford University Press (OUP)
Published: 2011-02-01
Volume: 186
Issue: 3
Pages: 1666-1674
ISSN: 0022-1767 (ISSN-L)
1550-6606
DOI: 10.4049/jimmunol.1002194
PMC: PMC4275066
OpenAlex: W2105431972
Cited by: 346
References: 57
Citations by year: 2026: 10 · 2025: 12 · 2024: 10 · 2023: 18 · 2022: 25 · 2021: 23 · 2020: 27 · 2019: 23 · 2018: 28 · 2017: 23 · 2016: 39 · 2015: 23 · 2014: 29 · 2013: 26 · 2012: 22
FWCI: 13.07
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations: The Journal of Immunology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (7r01hl079142-05)
National Heart, Lung, and Blood Institute (R01HL107380, R37HL079142, R01-HL079142)
Children's Hospital of Pittsburgh
Topics: Health Sciences › Medicine › Epidemiology › Influenza Virus Research Studies
Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Keywords: influenza A virus, Staphylococcus aureus, secondary bacterial pneumonia, Th17 response, IL-17, IL-22, IL-23, type I interferon, interferon-gamma, co-infection, hyper-IgE syndrome, STAT3, bacterial clearance, lung inflammation
MeSH terms: Interleukin-22, Animals, Cells, Cultured, T-Lymphocytes, Helper-Inducer, Humans, Interferon Type I, Interleukins, Mice, Inbred C57BL, Orthomyxoviridae Infections, Staphylococcal Infections, Staphylococcus aureus, Signal Transduction, Mice, Knockout, Pneumonia, Bacterial, Genetic Predisposition to Disease, Interleukin-17, Mice, Influenza A Virus, H1N1 Subtype, Interleukin-23

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Influenza A inhibits Th17-mediated host defense against bacterial pneumonia in mice.

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