Prostaglandin E2 receptor [EP2 subtype] contributes to jejunal dysmotility in schistosoma mansoni infected mice

ABSTRACT

Prostaglandin E2 [PGE2] is increased in inflammation and modulated intestinal peristalsis in the small intestine. However, the receptor mechanisms involved during parasitic inflammation are unknown. The aim of the present study was to investigate the role of EP2 receptors involved in the mechanisms underlying post-inflammatory changes during inflammation. Experiments were performed in male Swiss mice 4- and 8-wks following infection with S. mansoni and the results compared to those of uninfected control mice. Jejunal contraction was assessed using a modified Trendelenburg type preparation to study motor complexes [MCs]. Infection had great effects on jejunal motility that reflected by an increase of amplitude and a decrease of interval between MCs. EP2 receptor agonist AH 13205 [lO micro M] produced a significant inhibition of MCs which appeared as a decrease in amplitude and an increase in intervals in control, 4- and 8-wks infected animals. EP, and EP2 receptors antagonist AH6809 [30 micro M] attenuated intestinal peristalsis by a significant inhibition followed by contraction in control, 4- and 8-wks infected animals. In the presence of EP2 receptor antagonist AH6809, EP2 receptor agonist AH 13205 failed to alter the peristaltic motor activity in control, 4- and 8-wks infected jejunum. These data demonstrated temporal differences in motor function during the intensity of inflammation. EP2 receptor plays a potential role in modulating jejunal motility of control animals and altered motility triggered by parasitic inflammation