The Journal of Experimental Medicine
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Published online 6 August 2001. doi:10.1084/jem.194.3.355
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© The Rockefeller University Press, 0022-1007/2001/8/355/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 3, August 6, 2001 355-364

Original Article

Interleukin (IL)-18 Promotes the Development of Chronic Gastrointestinal Helminth Infection by Downregulating IL-13

Helena Helmbya, Kiyoshi Takedab, Shizuo Akirab, and Richard K. Grencisa
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

Correspondence to: Helena Helmby, School of Biological Sciences, Stopford Building 3.239, The University of Manchester, Manchester M13 9PT, UK. Tel:44-161-275-5319 Fax:44-161-275-5640 E-mail: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)-{gamma} 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-{gamma}.

In vivo treatment of T. muris–infected IFN-{gamma}–deficient mice with rIL-18 demonstrated that the inhibitory effect of IL-18 on IL-13 secretion is independent of IFN-{gamma}. Hence, IL-18 does not function as an IFN-{gamma}–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


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