Many of these defense mechanisms, such as peristalsis and tight junctions between intestinal epithelial cells [1], [3], [4], are abnormal or decreased in an immature intestine, and thus bacteria normally confined to the intestinal lumen are able to reach systemic organs and tissues.
An alteration of the cross-talk between intestinal epithelial cells and intraepithelial lymphocytes might actively contribute to the development of intestinal immune disorders, as occurring in patients with celiac disease.
To throughout dissect the cross-talk between intestinal epithelial cells and lymphocytes of both epithelium and lamina propria compartments, it is needful to understand the physiology of intestinal mucosa, as well as the development of intestinal inflammatory cascade occurring in common, and worldwide growing, intestinal disorders, as CD and IBD.
In an act of scientific serendipity, Fasano's group learned that this new enterotoxin could open the tight junctions between intestinal epithelial cells.
Considerable amounts of HRP were seen between intestinal epithelial cells only in mice treated with ETX, filtering through the tight junction, from the lumen of the bowel, towards the lamina propia (Fig. 5B).
The human intestinal microbiota has been shown to participate in epithelium maturation, host nutrition and protection against pathogens [11] and more recently in regulating gut epithelial cells proliferation [12], host energy metabolism [13] and immune responses [14], thus reflecting the symbiotic and beneficial crosstalk between intestinal epithelial cells (IECs) and intestinal microbiota.
A suitable and innovative method to evaluate the validity of such models for the 'normal' epithelium is by investigating similarities and differences in protein expression between cultured intestinal epithelial cells and epithelial scrapings obtained from human intestine.
The shell valves then open along the suture line and the binucleate germ cell penetrates between the intestinal epithelial cells of the worm.
Cell culture studies on the interaction between ST and intestinal epithelial cells have generally been performed with model that mimic enterocytes, i.e. the human colonic epithelial T84 cells.
The ability to restrain tolerogenic responses while permitting inflammatory responses requires communication between commensal bacteria, intestinal epithelial cells and immune cells.
However, there might be biomarkers even more suitable for this purpose and neither CEA nor CK20 discriminates between dislocated normal intestinal epithelial cells (iECs) and tumour cells with propensity to metastasize.
