| First Author | Chung CS | Year | 2001 |
| Journal | Am J Physiol Gastrointest Liver Physiol | Volume | 280 |
| Issue | 5 | Pages | G812-8 |
| PubMed ID | 11292588 | Mgi Jnum | J:69305 |
| Mgi Id | MGI:1934435 | Doi | 10.1152/ajpgi.2001.280.5.G812 |
| Citation | Chung CS, et al. (2001) Increased apoptosis in lamina propria B cells during polymicrobial sepsis is FasL but not endotoxin mediated. Am J Physiol Gastrointest Liver Physiol 280(5):G812-8 |
| abstractText | Recent studies from our laboratory demonstrated that mucosal lymphoid tissue such as Peyer's patch cells and lamina propria (LP) B lymphocytes from mice shows evidence of increased apoptosis after sepsis that is associated with localized inflammation/activation. The mechanism for this is poorly understood. Endotoxin as well as Fas/Fas ligand (FasL) have been shown to augment lymphocyte apoptosis; however, their contribution to the increase of apoptosis in LP B-cells during sepsis is not known. To study this, sepsis was induced by cecal ligation and puncture (CLP) in endotoxin-tolerant C3H/HeJ or FasL-deficient C3H/HeJ-FasL(gld) (FasL(-)) mice and LP lymphocytes were isolated 24 h later. Phenotypic, apoptotic, and functional indexes were assessed. The number of LP B cells decreased markedly in C3H/HeJ mice but not in FasL-deficient animals at 24 h after CLP. This was associated with comparable alteration in apoptosis and Fas antigen expression in the B cells of these mice. Septic LP lymphocytes also showed increased IgA production, which was absent in the FasL-deficient CLP mice. Furthermore, Fas ligand deficiency appeared to improve survival of septic challenge. These data suggest that the increase in B cell apoptosis in septic animals is partially due to a Fas/FasL-mediated process but not endotoxin. |
