Upon
infection with the cecum-dwelling nematode Trichuris muris, the majority of inbred strains of mice launch a Th2-type immune response and in doing so expel the parasite before patency. In contrast, there are a few mouse strains which develop a nonprotective Th1-type response resulting in a
chronic infection and the presence of adult worms. Of the Th2
cytokines known to be associated with the resistant phenotype (
interleukin-4 [IL-4], IL-5, IL-9, and
IL-13), comparatively little is known about the contribution that
IL-9 makes towards the protective immune response. In this study we demonstrate that
IL-9 is expressed early during the Th2-type response and that its elevation in vivo results in the enhancement of intestinal
mastocytosis and the production of both the
immunoglobulin E (
IgE) and
IgG1 isotypes. In addition, elevated
IL-9 levels in vivo facilitated the loss of T. muris from the intestine. That
IL-9 is important in promoting worm expulsion was also seen following
infection of IL-9-transgenic mice, which constitutively overexpress the
cytokine. These animals displayed an extremely rapid, but immune mediated, expulsion of the parasite. Also evident in these animals was a pronounced intestinal
mastocytosis, which was previously shown by us to be responsible for the expulsion of the related nematode Trichinella spiralis from these animals. Taken together with observations of
IL-9 production following
infection with other helminths, the results imply that
IL-9 contributes to the general mast cell and
IgE response characteristic of these
infections and, more specifically, enhances resistance to T. muris.