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Original Article

^a School of Biological Sciences, The University of Manchester, Manchester M13 9PT, UK
^b Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan
School of Biological Sciences, Stopford Building 3.239, The University of Manchester, Manchester M13 9PT, UK.44-161-275-564044-161-275-5319

helena.e.helmby{at}man.ac.uk

Expulsion of the gastrointestinal nematode Trichuris muris is mediated by a T helper (Th) 2 type response involving interleukin (IL)-4 and IL-13. Here we show that Th1 response–associated susceptibility involves prior activation of IL-18 and caspase-1 followed by IL-12 and interferon (IFN)- in the intestine. IL-18–deficient mice are highly resistant to chronic T. muris infection and in vivo treatment of normal mice with recombinant (r)IL-18 suppresses IL-13 and IL-4 secretion but does not affect IFN-.

In vivo treatment of T. muris–infected IFN-–deficient mice with rIL-18 demonstrated that the inhibitory effect of IL-18 on IL-13 secretion is independent of IFN-. Hence, IL-18 does not function as an IFN-–inducing cytokine during chronic T. muris infection but rather as a direct regulator of Th2 cytokines. These results provide the first demonstration of the critical role of IL-18 in regulating Th cell responses during gastrointestinal nematode infection.

Key Words: Th cell • cytokine • mucosa • nematode • regulation

© 2001 The Rockefeller University Press

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