Helminth-induced intestinal inflammation.
Gastrointestinal inflammation is a prominent feature of protective reactions in animals immune against helminths. Infiltration into the inflamed mucosa of various cells and their subsequent activation result in the elaboration of an array of pharmacologically and biologically active substances. The release of mediators is also associated with alterations in the epithelial layer. Furthermore, increased smooth muscle reactivity and enhanced secretory function of the mucosal tissue contribute to the development of an unfavourable environment and lead to worm expulsion. Mediators elaborated from inflammatory cells, whether associated with cell granules (i.e., preformed) or de novo-generated from membrane phospholipids, possess a number of potent vasoactive and spasmogenic properties which may contribute to events leading to worm elimination. The lipoxygenase metabolites of arachidonic acid (leukotrienes) derived from cell membranes probably contribute to the state of intestinal hypersensitivity against helminths. The measurement of elevated levels of these lipid mediators following worm challenge of immune, but not control, rats suggests that leukotrienes may play a role in amplifying and augmenting the inflammatory process associated with worm expulsion.
D000818:Animals; D004804:Eosinophils / Q000276:immunology; D006373:Helminthiasis / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology; D007249:Inflammation / Q000276:immunology; D007411:Intestinal Diseases, Parasitic / Q000276:immunology*; D007413:Intestinal Mucosa / Q000378:metabolism; D007975:Leukotriene B4 / Q000276:immunology; D008407:Mast Cells / Q000276:immunology; D009093:Mucus / Q000378:metabolism; D009130:Muscle, Smooth / Q000503:physiopathology; D009504:Neutrophils / Q000276:immunology; D051381:Rats; D013189:SRS-A / Q000276:immunology
D013189:SRS-A; D007975:Leukotriene B4; D007073:Immunoglobulin E