First Author | Gaddi PJ | Year | 2012 |
Journal | PLoS One | Volume | 7 |
Issue | 8 | Pages | e42850 |
PubMed ID | 22880122 | Mgi Jnum | J:189817 |
Mgi Id | MGI:5447091 | Doi | 10.1371/journal.pone.0042850 |
Citation | Gaddi PJ, et al. (2012) IL-10 mediated regulation of liver inflammation during acute murine cytomegalovirus infection. PLoS One 7(8):e42850 |
abstractText | Various cell types in both lymphoid and non-lymphoid tissues produce the anti-inflammatory cytokine interleukin (IL)-10 during murine cytomegalovirus (MCMV) infection. The functions of IL-10 in the liver during acute infection and the cells that generate this cytokine at this site have not been extensively investigated. In this study, we demonstrate that the production of IL-10 in the liver is elevated in C57BL/6 mice during late acute MCMV infection. Using IL-10 green fluorescence protein (GFP) reporter knock-in mice, designated IL-10-internal ribosomal entry site (IRES)-GFP-enhanced reporter (tiger), NK cells are identified as major IL-10 expressing cells in the liver after infection, along with T cells and other leukocytes. In the absence of IL-10, mice exhibit marked elevations in proinflammatory cytokines and in the numbers of mononuclear cells and lymphocytes infiltrating the liver during this infection. IL-10-deficiency also enhances liver injury without improving viral clearance from this site. Collectively, the results indicate that IL-10-producing cells in the liver provide protection from collateral injury by modulating the inflammatory response associated with MCMV infection. |