| First Author | Thiemann S | Year | 2017 |
| Journal | Cell Host Microbe | Volume | 21 |
| Issue | 6 | Pages | 682-694.e5 |
| PubMed ID | 28618267 | Mgi Jnum | J:357916 |
| Mgi Id | MGI:6284987 | Doi | 10.1016/j.chom.2017.05.005 |
| Citation | Thiemann S, et al. (2017) Enhancement of IFNgamma Production by Distinct Commensals Ameliorates Salmonella-Induced Disease. Cell Host Microbe 21(6):682-694.e5 |
| abstractText | The microbiota contributes to colonization resistance against invading pathogens by competing for metabolites, producing inhibitory substances, and priming protective immune responses. However, the specific commensal bacteria that promote host resistance and immune-mediated protection remain largely elusive. Using isogenic mouse lines with distinct microbiota profiles, we demonstrate that severity of disease induced by enteric Salmonella Typhimurium infection is strongly modulated by microbiota composition in individual lines. Transferring a restricted community of cultivable intestinal commensals from protected into susceptible mice decreases S. Typhimurium tissue colonization and consequently disease severity. This reduced tissue colonization, along with ameliorated weight loss and prolonged survival, depends on microbiota-enhanced IFNgamma production, as IFNgamma-deficient mice do not exhibit protective effects. Innate cells and CD4(+) T cells increase in number and show high levels of IFNgamma after transfer of the commensal community. Thus, distinct microbiota members prevent intestinal Salmonella infection by enhancing antibacterial IFNgamma responses. |
