ArticleImmunology letters2012
Potential role for alternatively activated macrophages in the secondary bacterial infection during recovery from influenza.
Article in Immunology letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
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- The Contribution of Viral Proteins to the Synergy of Influenza and Bacterial Co-Infection.Viruses · 2022Review
- Protection against influenza-induced Acute Lung Injury (ALI) by enhanced induction of M2a macrophages: possible role of PPARγ/RXR ligands in IL-4-induced M2a macrophage differentiation.Frontiers in immunology · 2022Article
- In Vitro Models for Studying Respiratory Host-Pathogen Interactions.Advanced biology · 2021Review
- Increased Pulmonary Pneumococcal Clearance after Resolution of H9N2 Avian Influenza Virus Infection in Mice.Infection and immunity · 2021Article
- Virus-Induced Changes of the Respiratory Tract Environment Promote Secondary Infections WithFrontiers in cellular and infection microbiology · 2021Review
- Early or Late Bacterial Lung Infection Increases Mortality After Traumatic Brain Injury in Male Mice and Chronically Impairs Monocyte Innate Immune Function.Critical care medicine · 2020Article
- SHP2 deficiency promotes Staphylococcus aureus pneumonia following influenza infection.Cell proliferation · 2020Article
- A Novel Role for PDZ-Binding Motif of Influenza A Virus Nonstructural Protein 1 in Regulation of Host Susceptibility to Postinfluenza Bacterial Superinfections.Viral immunology · 2019Article
- Mechanisms of Bacterial Superinfection Post-influenza: A Role for Unconventional T Cells.Frontiers in immunology · 2019Review
- Delayed oseltamivir plus sirolimus treatment attenuates H1N1 virus-induced severe lung injury correlated with repressed NLRP3 inflammasome activation and inflammatory cell infiltration.PLoS pathogens · 2018Article
- Aberrant Th2 inflammation drives dysfunction of alveolar macrophages and susceptibility to bacterial pneumonia.Cellular & molecular immunology · 2018Article
- Impaired expression of CXCL5 and matrix metalloproteinases in the lungs of mice with high susceptibility to Streptococcus pneumoniae infection.Immunity, inflammation and disease · 2018Article
- STAT2 Signaling Regulates Macrophage Phenotype During Influenza and Bacterial Super-Infection.Frontiers in immunology · 2018Article
- Overexpression of OSM and IL-6 impacts the polarization of pro-fibrotic macrophages and the development of bleomycin-induced lung fibrosis.Scientific reports · 2017Article
- The θ-defensin retrocyclin 101 inhibits TLR4- and TLR2-dependent signaling and protects mice against influenza infection.Journal of leukocyte biology · 2017Article
- Curcumin alleviates macrophage activation and lung inflammation induced by influenza virus infection through inhibiting the NF-κB signaling pathway.Influenza and other respiratory viruses · 2017Article
- First-Breath-Induced Type 2 Pathways Shape the Lung Immune Environment.Cell reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
purposeSecondary bacterial infections are a common complication of influenza. Innate immune host defenses appear to be impaired following influenza, leading to susceptibility to subsequent bacterial infections. Alternatively activated macrophages (AAM) in the lungs may play a critical role in eliciting the hypersusceptibility to secondary bacterial pneumonia.
methodsC57BL6 mice were challenged with sublethal doses of the mouse-adapted A/PR/8/34 (PR8) influenza virus or saline and allowed to recover. At complete recovery (day 14), mice were re-challenged with sublethal doses of Streptococcus pneumoniae serotype 3 (Sp3).
resultsPR8-recovered mice developed a rapidly fatal pulmonary infection to a 100-fold sublethal pneumococcal challenge, whereas PR8-naive mice demonstrated no mortality or illness. The cytokines which induce AAM (IL-4 and IL-13) and the expression of genes associated with AAM (Arginase-1, FIZZ1, and YM1) were elevated after PR8 infection. Flow cytometry suggests that alveolar macrophages demonstrate the AAM-phenotype, as indicated by MGL-1 and MHCII expression, in response to PR8 infection. Recovery from PR8 was associated with blunted cytokine responses to TLR ligands.
conclusionsThe mechanisms of immune regulation during recovery from influenza are being elucidated. We provide evidence that pulmonary AAM are induced during influenza infection and may contribute to the elicitation of hypersusceptibility to a secondary bacterial infection.
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