ArticleJournal of virology2012
Type I interferon induction during influenza virus infection increases susceptibility to secondary Streptococcus pneumoniae infection by negative regulation of γδ T cells.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
130 citing papers in PubMed, 191 citations in OpenAlex.
- Inflammation induced by influenza virus impairs human innate immune control of pneumococcus.Nature immunology · 2018Trial
- Myeloid cell reprogramming drives enhanced defense againstProceedings of the National Academy of Sciences of the United States of America · 2026Article
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Type I interferon signaling in hematopoietic cells impairs neutrophil antibacterial function in the middle ear during viral co-infection.Cell reports. Medicine · 2026Article
- Segmented filamentous bacteria reprogramming of alveolar macrophages limits postinfluenza bacterial pneumonia.Science immunology · 2026Article
- Current insights into bacterial secondary infection following influenza A virus infection.Frontiers in microbiology · 2026Review
- Influenza virus and Staphylococcus aureus super-infection disrupts spatially coordinated cellular immunity in the mouse lung.Communications biology · 2025Article
- Heterologous immunity and antibody-dependent enhancement in respiratory virus infections.Molecular biology reports · 2025Review
- Epigenetic changes and serotype-specific responses of alveolar type II epithelial cells to Streptococcus pneumoniae in resolving influenza A virus infection.Cell communication and signaling : CCS · 2025Article
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
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- Metabolomic and microbiome analysis of the protective effects of Puerarin against Salmonella Enteritidis Infection in chicks.BMC veterinary research · 2023Article
- Article
- Type-I interferons promote innate immune tolerance in macrophages exposed to Mycobacterium ulcerans vesicles.PLoS pathogens · 2023Article
- Antigen-specific memory Th17 cells promote cross-protection against nontypeable Haemophilus influenzae after mild influenza A virus infection.Mucosal immunology · 2023Article
- Human metapneumovirus driven IFN-β production antagonizes macrophage transcriptional induction of IL1-β in response to bacterial pathogens.Frontiers in immunology · 2023Article
- Interactions between the NLRP3-Dependent IL-1β and the Type I Interferon Pathways in Human Plasmacytoid Dendritic Cells.International journal of molecular sciences · 2022Article
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- Exposing the Two Contrasting Faces of STAT2 in Inflammation.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2022Review
- Heterotypic Influenza Infections Mitigate Susceptibility to Secondary Bacterial Infection.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
70 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.