The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Type I Interferon Induction during Influenza Virus Infection Increases Susceptibility to Secondary Streptococcus pneumoniae Infection by Negative Regulation of γδ T Cells
Open accessAbstract
The majority of deaths following influenza virus infection result from secondary bacterial superinfection, most commonly caused by Streptococcus pneumoniae . Several models have been proposed to explain how primary respiratory viral infections exacerbate secondary bacterial disease, but the mechanistic explanations have been contradictory. In this study, mice were infected with S. pneumoniae at different days after primary influenza A (X31) virus infection. Our findings show that the induction of type I interferons (IFNs) during a primary nonlethal influenza virus infection is sufficient to promote a deadly S. pneumoniae secondary infection. Moreover, mice deficient in type I interferon receptor (IFNAR knockout [KO] mice) effectively cleared the secondary bacterial infection from their lungs, increased the recruitment of neutrophils, and demonstrated an enhanced innate expression of interleukin-17 (IL-17) relative to wild-type (WT) mice. Lung γδ T cells were responsible for almost all IL-17 production, and their function is compromised during secondary S. pneumoniae infection of WT but not IFNAR KO mice. Adoptive transfer of γδ T cells from IFNAR KO mice reduced the susceptibility to secondary S. pneumoniae infection in the lung of WT mice. Altogether, our study highlights the importance of type I interferon as a key master regulator that is exploited by opportunistic pathogens such as S. pneumoniae . Our findings may be utilized to design effective preventive and therapeutic strategies that may be beneficial for coinfected patients during influenza epidemics.
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Cites
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Cited by
Type I interferons in infectious disease
McNab, F., Mayer-Barber, K., Sher, A., Wack, A., & O'Garra, A. (2015) · Nature Reviews Immunology · doi:10.1038/nri3787 · Cited by 2,780
The co-pathogenesis of influenza viruses with bacteria in the lung.
McCullers, J. A. (2014) · Nature Reviews Microbiology · doi:10.1038/nrmicro3231 · Cited by 722
The immunology of influenza virus-associated bacterial pneumonia.
Robinson, K. M., Kolls, J. K., & Alcorn, J. F. (2015) · Current Opinion in Immunology · doi:10.1016/j.coi.2015.02.002 · Cited by 132
Type I interferons in bacterial infections: A balancing act
Kovarik, P., Castiglia, V., Ivin, M., & Ebner, F. (2016) · Frontiers in Immunology · doi:10.3389/fimmu.2016.00652 · Cited by 117
Lung‐resident γδ T cells and their roles in lung diseases
Cheng, M., & Hu, S. (2017) · Immunology · doi:10.1111/imm.12764 · Cited by 108
Metadata
- Authors
- Li, W., Moltedo, B., & Moran, T. M.
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2012-11-15
- Volume
- 86
- Issue
- 22
- Pages
- 12304-12312
- ISSN
- 0022-538X (ISSN-L)
- 1098-5514
- OpenAlex
- W2006425559
- Cited by
- 194
- References
- 11
- FWCI
- 6.90
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Type I Interferon Induction during Influenza Virus Infection Increases Susceptibility to Secondary Streptococcus pneumoniae Infection by Negative Regulation of γδ T Cells. https://app.cochat.ai/papers/10.1128/jvi.01269-12
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- Li, W., Moltedo, B., & Moran, T. M. (2012). Type I Interferon Induction during Influenza Virus Infection Increases Susceptibility to Secondary Streptococcus pneumoniae Infection by Negative Regulation of γδ T Cells. Journal of Virology. https://doi.org/10.1128/jvi.01269-12
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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