Structural and molecular changes in intestinal smooth muscle induced by Trichinella spiralis infection

Abstract

Infection with Trichinella spiralis in the rat causes altered intestinal motility and jejunal smooth muscle contractility by day 6 postinoculation. The purpose of this study was to determine structural and molecular changes in the smooth muscle that could account for the functional changes that have been reported. By day 6 postinoculation, there was an increase in thickness of both muscle layers of the jejunum. This increase in mass was accompanied by an increase in total protein content of the seromuscular tissues. When specific proteins were analyzed, increases in actin and myosin heavy chain contents were found. On the other hand, there was no increase in collagen content. Alterations in gene expression at the pretranslational level were determined by monitoring total RNA and the proportion of mRNA that codes for alpha-smooth muscle actin. There was an increase in both parameters in longitudinal muscle from the jejunum of infected animals. The increase appeared to be site selective because there were no increases in either parameter in longitudinal muscle of the distal intestine. These results indicate that pretranslational upregulation of gene expression for actin isoforms occurs in smooth muscle of the proximal but not distal intestine during the early enteric phase of infection with T. spiralis. Thus the altered smooth muscle contractility that has been reported in experimental trichinosis may be related in part to an increased expression of smooth muscle protein.

How to express pharmacological contractions of the inflamed rat intestine

“…In our study, morphological analysis of the rat ileum showed that the longitudinal muscle layer accounted for about one-third of the muscularis propria. This is comparable with the findings of Weisbrodt et al (1994), who studied the muscle thickness of rat jejunum (Weisbrodt et al 1994). The density is assumed to be 1.05 mg/mm 3 (Keatinge 1968;Gordon and Siegman 1971).…”

“…Morphological hallmarks of chronic intestinal inflammation are hypertrophy (increased cell size) and hyperplasia (increased cell number) of the muscular layers (Castro 1989;Blennerhassett et al 1992;Weisbrodt et al 1994). Since the contractile capacity of the longitudinal muscle layer is directly proportional to the muscle mass, the overall smooth muscle contractility of chronically inflamed intestine is increased.…”

Microarray analysis of selection lines from outbred populations to identify genes involved with nematode parasite resistance in sheep

“…Also in mouse, it has been shown that CD4ϩ T-cells and MHC class II expression influence worm expulsion and increased intestinal muscle contraction during T. spiralis infection (61). Although this is the first time that TAGLN has been associated with the response to gastrointestinal parasites, the increase of other smooth muscle-specific proteins after nematode infection (in particular, actin and myosin heavy chain) was shown by Weisbrodt et al (64). In addition, this work showed pretranslational upregulation of gene expression for actin isoforms at the infection area.…”

Cytoskeleton remodeling and alterations in smooth muscle contractility in the bovine jejunum during nematode infection

“…In the ratTrichinella spiralis system, an increase in thickness of jejunal smooth muscle layers as a result of experimental infection is observed at 6 days. This increase is accompanied with an increase in total protein of seromuscular tissues, as well as actin and myosin heavy chain at both mRNA and protein levels (Weisbrodt et al 1994). Infection-induced changes in smooth muscle appear to occur in the proximal but not distal intestine (colon).…”