Enhanced intestinal motor response to cholecystokinin in post-Nippostrongylus brasiliensis-infected rats: modulation by CCK receptors and the vague nerve

The jejunal inflammation induced in rats by the nematode Nippostrongylus br asiliensis is followed by intestinal neuroimmune alterations including mast cell hyperplasia and nerve remodelling. On the other hand, cholecystokinin (CCK) plays a pivotal role in the regulation of intestinal motility. The a im of this study was To determine whether the intestinal motor response to CCK is altered 30 days after infection by N. brasiliensis. Thus, CCK-8 (50 mug kg(-1) intraperitoneally) disrupted the pattern of jejunal migrating my oelectric complexes for a longer time in postinfected rats (95.5 +/- 3.5 mi n) than in controls (48.1 +/- 5.1 min). This enhanced jejunal response was also found after oral administration of the potent releaser of endogenous C CK, soybean trypsin inhibitor. In contrast, no alteration of the inhibition of colonic motility by CCK administration was observed. The increased resp onsiveness of jejunal motility so CCK persisted after mast cell stabilisati on or depletion bur was prevented by atropine, devazepide and L-365260 (CCK -A and CCK-B receptor antagonists, respectively) and vagotomy. These result s indicate that neuroimmune alterations after N. brasiliensis infection lea d to an increased intestinal motility response to CCK that involves a choli nergic mediation, a vagal pathway and alterations in intestinal CCK-A and C CK-B receptors.