| First Author | Hiromatsu T | Year | 2003 |
| Journal | Eur J Immunol | Volume | 33 |
| Issue | 9 | Pages | 2511-9 |
| PubMed ID | 12938227 | Mgi Jnum | J:85452 |
| Mgi Id | MGI:2675203 | Doi | 10.1002/eji.200324077 |
| Citation | Hiromatsu T, et al. (2003) NK T cells stimulated with a ligand for TLR2 at least partly contribute to liver injury caused by Escherichia coli infection in mice. Eur J Immunol 33(9):2511-9 |
| abstractText | Fas ligand (Fas L) expression was induced on intrahepatic NK1.1(+) T cells in vivo after an intraperitoneal inoculation of Escherichia coli. Liver injury after E. coli infection, as assessed by serum GPT level and histological examination, was significantly reduced in Jalpha281(-/-) mice lacking NK1.1(+) T cells or in gld/gld mice bearing mutated Fas L, indicating that NK T cells at least partly contribute to E. coli-induced liver injury in a Fas/Fas L-dependent manner. Bacterial numbers in organs and cytokine levels in serum of Jalpha281(-/-) mice did not differ from those of Jalpha281(+/+) mice following E. coli infection. Intrahepatic NK1.1(+) T cells, which preferentially expressed Toll-like receptor 2 (TLR2) mRNA, responded in vitro to synthetic lipoprotein, a ligand for TLR2, by inducing Fas L expression on their surface. In a manner analogous to E. coli infection, lipoprotein and LPS could additively induce Fas L expression on NK1.1(+) T cells, leading to liver injury in vivo in normal mice but not in gld/gld mice. In conclusion, it is suggested that induction of Fas L on NK T cells in response to bacterial components such as lipoproteins plays an important role in pathogenesis of E. coli-induced liver injury in mice. |
