| First Author | Yajima T | Year | 2004 |
| Journal | Infect Immun | Volume | 72 |
| Issue | 7 | Pages | 3855-62 |
| PubMed ID | 15213127 | Mgi Jnum | J:90998 |
| Mgi Id | MGI:3045651 | Doi | 10.1128/IAI.72.7.3855-3862.2004 |
| Citation | Yajima T, et al. (2004) Overexpression of Interleukin-15 increases susceptibility to lipopolysaccharide-induced liver injury in mice primed with Mycobacterium bovis bacillus Calmette-Guerin. Infect Immun 72(7):3855-62 |
| abstractText | Mice primed with Mycobacterium bovis bacillus Calmette-Guerin (BCG) are highly sensitive to lipopolysaccharide (LPS)-induced liver injury and lethality. We found that interleukin-15 (IL-15) transgenic (Tg) mice primed with BCG were more susceptible to LPS-induced liver injury than non-Tg mice. The numbers of CD44+ CD8+ T cells expressing intracellular gamma interferon (IFN-gamma) significantly increased in the livers of BCG-primed IL-15 Tg mice after LPS injection, and the depletion of CD8+ T cells from BCG-primed IL-15 Tg mice completely abolished the susceptibility to LPS-induced lethality. Liver T cells from BCG-primed IL-15 Tg mice produced IFN-gamma in vitro in response to LPS, which was inhibited by the addition of anti-IL-12 monoclonal antibody (MAb). In vivo treatment with anti-IL-12 MAb inhibited the appearance of CD44+ CD8+ T cells expressing intracellular IFN-gamma after LPS injection. These results suggest that the overexpression of IL-15 increases susceptibility to LPS-induced liver injury in BCG-primed mice via bystander activation of CD8+ T cells. |
