Authors
Oliver Liesenfeld, Hoil Kang, Daniel Park, Thu A Nguyen, Chandan V Parkhe, Hisami Watanabe, Toru Abo, Alan Sher, Jack S Remington, Yasuhiro Suzuki
Publication date
1999/7
Journal
Parasite immunology
Volume
21
Issue
7
Pages
365-376
Publisher
Blackwell Science Ltd
Description
We previously reported that genetic susceptibility of mice to peroral infection with T. gondii is associated with CD4+ T cell‐dependent, interferon (IFN)‐γ‐mediated necrosis of their small intestine. We examined the role of tumour necrosis factor (TNF)‐α and nitric oxide (NO), in addition to IFN‐γ. At 7 days after infection, a marked increase in CD4+ T cells was observed in lamina propria mononuclear cells (LPC) of the small intestine as compared with normal mice, and significantly greater amounts of mRNA for IFN‐γ, TNF‐α, and inducible NO synthase (iNOS) were detected in LPC of the small intestine of infected than uninfected animals. Treatment of infected mice with anti‐TNF‐α monoclonal antibody (mAb) or the iNOS inhibitor, aminoguanidine, prevented necrosis and prolonged time to death. Infected iNOS‐targeted mutant mice did not develop the disease whereas infected, control mice did. Treatment with anti …
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