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(American Journal of Pathology. 2006;169:1701-1712.)
© 2006 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2006.060346

TH1-Dominant Granulomatous Pathology Does Not Inhibit Fibrosis or Cause Lethality during Murine Schistosomiasis

Mosiuoa Leeto, De’Broski R. Herbert, Reece Marillier, Anita Schwegmann, Lizette Fick and Frank Brombacher

From the Division of Infectious Immunology, University of Cape Town, Cape Town, South Africa

Schistosoma mansoni egg-induced inflammation is accompanied by TH2 cell polarization and development of fibrotic granulomas in host tissue. The interleukin (IL)-4 receptor {alpha} (IL-4R{alpha}), 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-4R{alpha}-deficient mice (LckCreIL-4R{alpha}–/lox) developed granulomas and egg-driven collagen production. Although eosinophilia and goblet cell hyperplasia were impaired in LckCreIL-4R{alpha}–/lox mice, there was no reduction in size or collagen content of lung and liver granulomas. The lack of CD4+ T-cell IL-4R{alpha} 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 TH1-associated liver injury did not lead to premature mortality in this strain. Instead, lower levels of serum endotoxin in LckCreIL-4R{alpha}–/lox mice suggest that intestinal barrier function may be the dominant factor for survival during natural infection.




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