Beta1 integrins are anchored on the basal membrane of enterocytes, but little is known about their localization in M cells, which are the main entry route into the intestinal mucosa for many ...bacterial pathogens. In particular, it has been suggested that adhesion of enteropathogenic Yersinia to M cells is mediated by interaction of the bacterial protein invasin and apical beta1 integrins. Using a novel in vitro model of M cells, we demonstrate an augmented apical and basolateral targeting of beta1 integrins in M cells associated with increased total alpha chain synthesis. The alpha3 and alpha6 subunits were targeted to the basal pole, but alpha2 subunit was targeted at both poles. No other alpha subunit was found associated with apical beta1 integrins on M cells. Interestingly, Y. enterocolitica still adhered to the apical surface of M cells, despite the fact that alpha2beta1 is not a receptor for invasin. We therefore studied the adhesive properties of invasin-mutant Y. enterocolitica and invasin-expressing Escherichia coli on the apical surface of M cells. We show that it is not invasin, but the product of an as yet unidentified bacterial chromosomal gene, that is involved in the adhesion of Y. enterocolitica to the apical membrane of M cells.
Differentiation of specific epithelial cell lineages during development, as well as epithelial plasticity in response to heterologous cell‐to‐cell cross talk during adult life, accounts for the large ...variety of functions which are performed by the mucosal surfaces found in the human body. Among its functions, the digestive mucosa is able to sample antigens and microorganisms through M cells of Peyer's patches follicle‐associated epithelium, in order to trigger the development of either tolerance or immune responses. At least in the gut, M‐cell formation is immunoregulated. Close contact between immune cells and intestinal epithelium modifies the permeability of the epithelial barrier by inducing the conversion of enterocytes into M cells, offering at the same time an opportunistic way of invasion for pathogens. These lympho‐epithelial interactions triggering M‐cell formation have now been modeled in culture.
