| First Author | La Flamme AC | Year | 2001 |
| Journal | Infect Immun | Volume | 69 |
| Issue | 12 | Pages | 7445-52 |
| PubMed ID | 11705919 | Mgi Jnum | J:73134 |
| Mgi Id | MGI:2154609 | Doi | 10.1128/IAI.69.12.7445-7452.2001 |
| Citation | La Flamme AC, et al. (2001) Role of gamma interferon in the pathogenesis of severe schistosomiasis in interleukin-4-deficient mice. Infect Immun 69(12):7445-52 |
| abstractText | In the absence of interleukin-4 (IL-4), infection with Schistosoma mansoni leads to a severe fatal disease rather than the chronic survivable condition that occurs in wild-type (WT) mice. Because the sustained production of NO most closely correlates to weight loss and fatality in infected IL-4(-/-) mice and because gamma interferon (IFN-gamma) is an important inducer of inducible NO synthase, infected IL-4(-/-) mice were treated with anti-IFN-gamma antibodies to determine the role of IFN-gamma during schistosomiasis in WT and IL-4(-/-) animals. When IFN-gamma was neutralized, Th2 responses were enhanced and NO production was reduced in both WT and IL-4(-/-) mice. The decreased NO production correlated with a rescue of proliferation in splenocytes from infected IL-4(-/-) mice. Furthermore, the neutralization of IFN-gamma in vivo improved the gross appearance of the liver and led to a reduction in granuloma size in infected IL-4(-/-) but not WT mice. However, the neutralization of IFN-gamma in vivo did not affect the development of severe disease in infected IL-4(-/-) mice. These results suggest that while the increased production of IFN-gamma does lead to some of the pathology observed in infected IL-4(-/-) mice, it is not ultimately responsible for cachexia and death. |
