Expression and distribution of beta1 integrins in in vitro-induced M cells: implications for Yersinia adhesion to Peyer's patch epithelium.

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.

Interaction of pathogenic bacteria with rabbit appendix M cells: bacterial motility is a key feature in vivo.

Rabbit appendix consists mainly of lymphoid follicles (LF) covered by M cells, the specialized antigen-sampling cells of the mucosal immune system, and surrounded by glandular epithelium. Until now, these M cells have been characterized morphologically and histologically by using cellular markers. Here, the adhesion and transport of pathogenic bacteria were investigated to assess the function of M cells of the appendix.

Chronic acid exposure leads to activation of the cdx2 intestinal homeobox gene in a long-term culture of mouse esophageal keratinocytes.

To explore mechanisms whereby Malpighian keratinocytes can transdifferentiate into an intestinal-like epithelium, as observed in the early steps of Barrett's esophagus (BE) development, long-standing cultures of esophageal keratinocytes derived from normal mouse esophageal explants were developed. These cells were able to form multilayers and to differentiate on filter support by the formation of differentiated layers of basal cells (cytokeratine 14 positive) on which secondary suprabasal cell layers (cytokeratine 4 positive) spontaneously developed. Thus, these cultured cells, referred to as P3E6, reproduced, at least in part, the proliferation and stratification pattern existing in the normal esophagus.

Poliovirus transcytosis through M-like cells.

During the digestive-tract phase of infection, poliovirus (PV) is found in the oropharynx and the intestine. It has been proposed that PV enters the organism by crossing M cells, which are scattered in the epithelial sheet covering lymphoid follicles of Peyer's patches. However, PV translocation through M cells has never been demonstrated.

Lymphoepithelial interactions trigger specific regulation of gene expression in the M cell-containing follicle-associated epithelium of Peyer's patches.

In the intestine, the follicle-associated epithelium (FAE) of Peyer's patches (PP) performs Ag sampling as the first step in developing immune responses. Depending on the species, this epithelium contains 10-50% of M cells, which act as regulated gates in epithelial barriers that can be used opportunistically by pathogens to invade their host. However, the mechanisms involved in the differentiation and uptake processes of M cells are not known, in part because their limited number in the intestinal mucosa has hampered molecular and biochemical studies.