| First Author | Li N | Year | 2020 |
| Journal | iScience | Volume | 23 |
| Issue | 12 | Pages | 101767 |
| PubMed ID | 33251497 | Mgi Jnum | J:307326 |
| Mgi Id | MGI:6705725 | Doi | 10.1016/j.isci.2020.101767 |
| Citation | Li N, et al. (2020) Flu Virus Attenuates Memory Clearance of Pneumococcus via IFN-gamma-Dependent Th17 and Independent Antibody Mechanisms. iScience 23(12):101767 |
| abstractText | 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-gamma-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-gamma. 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. |
