M cells as ports of entry for enteroinvasive pathogens: mechanisms of interaction, consequences for the disease process

Semin Immunol. 1999 Jun;11(3):193-203. doi: 10.1006/smim.1999.0175.

Abstract

M cells are key sites of antigen sampling for the mucosal-associated lymphoid system (MALT) and consequently are essential components of the structures serving as inductive sites for mucosal immunity. In addition, they have recently been recognized as major sites of adherence and major ports of entry for enteric pathogens. In the case of enteroinvasive pathogens, such as Salmonella, Yersinia and Shigella, few clinical evidences, but lots of experimental data indicate that, at least at the early stage of infection, M cells of the follicular associated epithelium transport the pathogens. This has significantly altered our view on the pathogenesis of enteroinvasive infections. Crossing the epithelial barrier seems an achievable task for these bacteria which express adherence and invasion mechanisms which have often been well characterized in epithelial cell lines. These systems seem to be also used for entering and crossing M cells, although reproducible in vitro assays for M cell infection are now required. Having crossed the epithelial lining, the bacteria face phagocytic cells, particularly the macrophages that are present in the follicle dome. Depending on the capacity to survive in the presence of macrophages, and how this survival is achieved by a given invasive species, the outcome of infection can be dramatically affected. In consequence, M cells can be considered as pathogen translocators toward immunocompetent areas of the gut, thus opening the possibility to harness this property in order to design new mucosal vaccines or vaccine vectors.

Publication types

  • Review

MeSH terms

  • Antigens / metabolism
  • Biological Transport
  • Epithelial Cells / cytology*
  • Humans
  • Intestinal Mucosa / cytology
  • Intestinal Mucosa / microbiology
  • Intracellular Membranes / immunology
  • Phagocytosis

Substances

  • Antigens