Protective role of the epithelium of the small intestine and colon Academic Article uri icon

abstract

  • : The intestinal epithelium must selectively absorb nutrients but exclude luminal pathogens and pro-inflammatory molecules from host tissues. It is topographically organised with proliferating cells buried deep in the crypts and functionally mature cells lining the surface or villus. This ensures efficient barrier function at the interface and relative protection of stem cells from luminal insults. The rapid turnover of cells necessitates high energy requirements. Luminal glutamine and butyrate are necessary to maintain optimal energy status of the small and large intestinal epithelium, respectively. The passage of macromolecules across the epithelium is selectively impeded by enterocytes and intercellular tight junctions. Multiple factors have been recognised that alter paracellular permeability, but relatively little is known regarding control of transcellular passage of macromolecules. The intestinal epithelium is, however, more than just a physical barrier. It can detoxify xenobiotics. It secretes "protective" factors including immunoglobulins, mucus, trefoil peptides, and defensins into the lumen, while epithelial release of chemokines, cytokines, and other inflammatory mediators may initiate mucosal immunity or inflammation. The epithelial response to injurious stimuli is complex and may lead to events that, for example, enhance barrier function, reduce their susceptibility to injury, or recruit secondary protective mechanisms. The intestinal epithelium rapidly migrates across breeches in its continuity, a process that, in more severe injury, sets up a microenvironment more amenable to efficient regeneration. Repair events are also regulated at multiple levels. Thus, the complexity of the active and passive roles of the epithelial barrier in protecting the organism from its environment is now unfolding. The knowledge gained offers insight into pathogenesis of diseases such as inflammatory bowel disease and may form a rational basis for the future design of novel therapeutic strategies in their management.

publication date

  • 1996