| First Author | Biram A | Year | 2022 |
| Journal | Immunity | Volume | 55 |
| Issue | 3 | Pages | 442-458.e8 |
| PubMed ID | 35182483 | Mgi Jnum | J:328581 |
| Mgi Id | MGI:7281902 | Doi | 10.1016/j.immuni.2022.01.013 |
| Citation | Biram A, et al. (2022) Bacterial infection disrupts established germinal center reactions through monocyte recruitment and impaired metabolic adaptation. Immunity 55(3):442-458.e8 |
| abstractText | Consecutive exposures to different pathogens are highly prevalent and often alter the host immune response. However, it remains unknown how a secondary bacterial infection affects an ongoing adaptive immune response elicited against primary invading pathogens. We demonstrated that recruitment of Sca-1(+) monocytes into lymphoid organs during Salmonella Typhimurium (STm) infection disrupted pre-existing germinal center (GC) reactions. GC responses induced by influenza, plasmodium, or commensals deteriorated following STm infection. GC disruption was independent of the direct bacterial interactions with B cells and instead was induced through recruitment of CCR2-dependent Sca-1(+) monocytes into the lymphoid organs. GC collapse was associated with impaired cellular respiration and was dependent on TNFalpha and IFNgamma, the latter of which was essential for Sca-1(+) monocyte differentiation. Monocyte recruitment and GC disruption also occurred during LPS-supplemented vaccination and Listeria monocytogenes infection. Thus, systemic activation of the innate immune response upon severe bacterial infection is induced at the expense of antibody-mediated immunity. |
