Abstract
BackgroundThe intestinal epithelium plays a multifactorial role in mucosal defense. In this sense, augmented epithelial cell turnover appears as a potential effector mechanism for the rejection of intestinal-dwelling helminths.MethodsA BrdU pulse-chase experiment was conducted to investigate the infection-induced alterations on epithelial cell kinetics in hosts of high (mouse) and low (rat) compatibility with the intestinal trematode Echinostoma caproni.ResultsHigh levels of crypt-cell proliferation and tissue hyperplasia were observed in the ileum of infected mice, coinciding with the establishment of chronic infections. In contrast, the cell migration rate was about two times higher in the ileum of infected rats compared with controls, with no changes in tissue structure, indicating that an accelerated cell turnover is associated with worm expulsion.ConclusionOur results indicate that E. caproni infection induces a rapid renewal of the intestinal epithelium in the low compatible host that may impair the establishment of proper, stable host-parasite interactions, facilitating worm clearance.
Highlights
The intestinal epithelium plays a multifactorial role in mucosal defense
Levels of intestinal epithelial cell proliferation The levels of IEC undergoing proliferation were assessed on sections from animals necropsied 1 h post administration of BrdU
Our study revealed that E. caproni infection induced a marked alteration of intestinal tissue structure in the ileum of infected mice, which was characterized by tissue hyperplasia
Summary
The intestinal epithelium plays a multifactorial role in mucosal defense In this sense, augmented epithelial cell turnover appears as a potential effector mechanism for the rejection of intestinal-dwelling helminths. Intestinal-dwelling helminths maintain an intimate contact with the intestinal epithelium, alterations in the intestinal architecture and/or homeostasis affect their microhabitat and can compromise the stability of parasites located at this environment. These changes are normally under the control of the immune system, which is able to manage a vast number of effector mechanisms that are directed to degrade, disable and/or dislodge intestinal helminths with the ultimate aim of inducing their expulsion from the host organism. The use of host-parasite systems that display different immune responses and susceptibility to infection arises as a useful approach to investigate the way these mechanisms can influence the course of the infection
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