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Both IL‐12 and IL‐18 contribute to small intestinal Th1‐type immunopathology following oral infection with Toxoplasma gondii, but IL‐12 is dominant over IL‐18 in parasite control

Oral infection of C57BL/6 mice with Toxoplasma gondii results in small intestinal Th1‐type immunopathology mediated by local production of IFN‐γ, TNF‐α, and NO. To analyze whether the proinflammatory cytokines IL‐12 and IL‐18 play a role in the induction of immunopathology, IL‐12p35/p40–/– and IL‐18–/– mice were orally infected with T. gondii. Wild‐type mice developed massive necrosis in their small intestines and died 7–10 days post infection. Even though IL‐12p35/40–/– mice did not develop the necrosis they all died between day 9 and 11 after infection. In contrast, 50% of IL‐18–/– mice died during the acute phase of infection. Compared to wild‐type mice, IL‐12p35/p40–/– but not IL‐18–/– mice showed significantly higher parasite numbers in their small intestines and significantly higher numbers of parasite‐associated inflammatory foci in their livers. IFN‐γ production was similar in infected wild‐type and IL‐18–/– mice but significantly decreased in IL‐12p35/p40–/– mice. Treatment of mice with anti‐IL‐12‐ or anti‐IL‐18 antibodies after infection prevented the development of intestinal necrosis. These results reveal that both IL‐12 and IL‐18 play an important role in the development of intestinal immunopathology following oral infection with T. gondii. However, IL‐12 is dominant over IL‐18 in the host defense against parasite replication. Therefore, neutralization of IL‐18 (rather than TNF‐α, IL‐12, and IFN‐γ) may be a safe strategy for the treatment of Th1‐associated diseases.