Alterations of intestinal motor responses to various stimuli after Nippostrongylus brasiliensis infection in rats: role of mast cells

Abstract

Nippostrongylus brasiliensis infection induces jejunal mastocytosis associated with enteric nerve remodelling in rats. The aim of this study was to evaluate the intestinal motility responses to meals and to neurotransmitters involved in the control of gut motility (acetylcholine (carbachol), substance P and neurokinin A) in both control and N. brasiliensis-infected rats 30 days post-infection. All rats were equipped with NiCr electrodes in the jejunum to record myoelectrical activity. The duration of disruption of the jejunal migrating myoelectrical complexes (MMC) induced by the different stimuli was determined. Meal ingestion and substance P administration disrupted the MMC pattern for similar durations in the two groups. Carbachol and neurokinin A induced a significantly longer MMC disruption in post-infected rats than in controls (125 +/- 8.3 vs. 70 +/- 6 min for carbachol 100 microg kg-1 and 51 +/- 4 vs. 40 +/- 2 for neurokinin A 50 microg kg-1). The enhanced motor response in postinfected rats was reduced by previous mast cell stabilization with ketotifen or mast cell degranulation with compound BrX 537 A. In conclusion, the increased intestinal motor reactivity to carbachol and neurokinin A in post-N. brasiliensis-infected rats depends upon intestinal mast cell hyperplasia and degranulation.

Changes in Interstitial Cells of Cajal at the Deep Muscular Plexus Are Associated with Loss of Distention-Induced Burst-Type Muscle Activity in Mice Infected by Trichinella spiralis

“…In contrast to a T. spiralis infection in which macrophages are the dominant immune cell in the musculature, mast cells penetrated the musculature after a N. brasiliensis infection 45 and changes in motor function in response to a N. brasiliensis infection depended on the presence of mast cells. 46 Interestingly, the presence of mast cells in the musculature was long lasting with a half life of 40 days, which may explain the severity of the damage to ICC. 45 The present study provides further evidence for the T. Spiralis-infected mouse being a model for postinfectious enteropathies, a significant problem in clinical gastroenterology.…”

Pathogenesis of irritable bowel syndrome: The mast cell connection

“…In the small bowel, this inhibition is mediated by histamine, 5-HT and prostaglandins and leukotrienes, whereas in the colon inhibition is mediated mainly by 5-HT3 receptors, substance P and vagal afferents [120]. In the parasite model, in the post-infection phase, an enhanced motor response to carbachol and neurokinin A develops and this response is also mast celldependent [121].…”

Mast Cell Stabilizer Ketotifen [4-(1-Methyl-4-piperidylidene)-4H-benzo[4,5]cyclohepta[1,2-b]thiophen-10(9H)-one Fumarate] Prevents Mucosal Mast Cell Hyperplasia and Intestinal Dysmotility in Experimental Trichinella spiralis Inflammation in the Rat

“…Several studies correlate mast cell activity with the development of functional disorders such as alteration of intestinal permeability (Santos et al, 2001), motor disorders (Gay et al, 2000a), and visceral hypersensitivity (Kreis et al, 1998). We previously demonstrated that activation of mast cells could modify intestinal motility, even in the absence of apparent intestinal inflammation (Saavedra and Vergara, 2005).…”