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Flu Virus Attenuates Memory Clearance of Pneumococcus via IFN-γ-Dependent Th17 and Independent Antibody Mechanisms
Bacterial coinfection is a major cause of influenza-associated mortality. Most people have experienced infections with bacterial pathogens commonly associated with influenza A virus (IAV) coinfection before IAV exposure; however, bacterial clearance through the immunological memory response (IMR) in...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7683269/ https://www.ncbi.nlm.nih.gov/pubmed/33251497 http://dx.doi.org/10.1016/j.isci.2020.101767 |
Sumario: | Bacterial coinfection is a major cause of influenza-associated mortality. Most people have experienced infections with bacterial pathogens commonly associated with influenza A virus (IAV) coinfection before IAV exposure; however, bacterial clearance through the immunological memory response (IMR) in coinfected patients is inefficient, suggesting that the IMR to bacteria is impaired during IAV infection. Adoptive transfer of CD4(+) T cells from mice that had experienced bacterial infection into IAV-infected mice revealed that memory protection against bacteria was weakened in the latter. Additionally, memory Th17 cell responses were impaired due to an IFN-γ-dependent reduction in Th17 cell proliferation and delayed migration of CD4(+) T cells into the lungs. A bacterium-specific antibody-mediated memory response was also substantially reduced in coinfected mice, independently of IFN-γ. These findings provide additional perspectives on the pathogenesis of coinfection and suggest additional strategies for the treatment of defective antibacterial immunity and the design of bacterial vaccines against coinfection. |
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