Eosinophilic leukocytes function in host protection against parasitic worms. In turn, helminthic parasites harbor specific molecules to evade or paralyze eosinophil-associated host immune responses; these molecules facilitate the migration and survival of parasitic helminths in vivo. This competition between eosinophil and worm leads to stable equilibria between them. An understanding of such dynamic host-eosinophil interactions will help us to uncover mechanisms of cross talk between host and parasite in helminth infection. In this review, we examine recent findings regarding the innate immune responses of eosinophils to helminthic parasites, and discuss the implications of these findings in terms of eosinophil-mediated tissue inflammation in helminth infection.
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Eosinophil degranulation plays a crucial role in tissue inflammatory reactions associated with helminth parasitic infections and allergic diseases.
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Eosinophil degranulation is considered to be a key effector function for the killing of helminthic worms and tissue inflammation at worm-infected lesion sites. However, relatively little data are available with regard to eosinophil response after stimulation with worm-secreted products which contain a large quantity of cysteine proteases. In this study, we attempted to determine whether the degranulation of human eosinophils could be induced by the direct stimulation of the excretory-secretory products (ESP) of
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To examine the fate of
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The last two decades witnessed significant advances in the efforts of immunoparasitologists to elucidate the nature and role of the host mucosal defence mechanisms against intestinal nematode parasites. Aided by recent advances in basic immunology and biotechnology with the concomitant development of well defined laboratory models of infection, immunoparasitologists have more precisely analyzed and defined the different immune effector mechanisms during the infection; resulting in great improvement in our current knowledge and understanding of protective immunity against gastrointestinal (GI) nematode parasites. Much of this current understanding comes from experimental studies in laboratory rodents, which have been used as models of livestock and human GI nematode infections. These rodent studies, which have concentrated on
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Eosinophil and IgE responses of interleukin (IL)-5 transgenic and normal C3H/HeN mice were studied after experimental infection with
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