| First Author | Leeto M | Year | 2006 |
| Journal | Am J Pathol | Volume | 169 |
| Issue | 5 | Pages | 1701-12 |
| PubMed ID | 17071593 | Mgi Jnum | J:114570 |
| Mgi Id | MGI:3689450 | Doi | 10.2353/ajpath.2006.060346 |
| Citation | Leeto M, et al. (2006) TH1-Dominant Granulomatous Pathology Does Not Inhibit Fibrosis or Cause Lethality during Murine Schistosomiasis. Am J Pathol 169(5):1701-12 |
| abstractText | Schistosoma mansoni egg-induced inflammation is accompanied by T(H)2 cell polarization and development of fibrotic granulomas in host tissue. The interleukin (IL)-4 receptor alpha (IL-4Ralpha), which mediates IL-4 and IL-13 signaling, is essential for granulomatous pathology through a putative CD4(+) T-cell-dependent mechanism. In this study, we asked whether CD4(+) T-cell-specific IL-4Ralpha-deficient mice (Lck(Cre)IL-4Ralpha(-/lox)) developed granulomas and egg-driven collagen production. Although eosinophilia and goblet cell hyperplasia were impaired in Lck(Cre)IL-4Ralpha(-/lox) mice, there was no reduction in size or collagen content of lung and liver granulomas. The lack of CD4(+) T-cell IL-4Ralpha expression caused significant increases in interferon-gamma-producing cells, inducible nitric-oxide synthetase production, and hepatic damage, compared with similarly infected wild-type mice. Interestingly, this T(H)1-associated liver injury did not lead to premature mortality in this strain. Instead, lower levels of serum endotoxin in Lck(Cre)IL-4Ralpha(-/lox) mice suggest that intestinal barrier function may be the dominant factor for survival during natural infection. |
