Article Text

Download PDFPDF
Intestinal epithelial responses to enteric pathogens: effects on the tight junction barrier, ion transport, and inflammation

Abstract

The effects of pathogenic organisms on host intestinal epithelial cells are vast. Innumerable signalling pathways are triggered leading ultimately to drastic changes in physiological functions. Here, the ways in which enteric bacterial pathogens utilise and impact on the three major physiological functions of the intestinal epithelium are discussed: alterations in the structure and function of the tight junction barrier, induction of fluid and electrolyte secretion, and activation of the inflammatory cascade. This field of investigation, which was virtually non-existent a decade ago, has now exploded, thus rapidly expanding our understanding of bacterial pathogenesis. Through increased delineation of the ways in which microbes alter host physiology, we simultaneous gain insight into the normal regulatory mechanisms of the intestinal epithelium.

  • tight junctions
  • enteric pathogens
  • ion transport
  • epithelium
  • inflammation
  • TJ, tight junctions
  • TER, transepithelial electrical resistance
  • PKC, protein kinase C
  • PKCα, protein kinase Cα
  • PKCβ, protein kinase Cβ
  • EPEC, entero-pathogenic Escherichia coli
  • MLCK, myosin light chain kinase
  • EHEC, enterohaemorrhagic Escherichia coli
  • BFT, B fragilis enterotoxin
  • Isc, short circuit current
  • HA/P, haemagglutinin protease
  • CPE, C perfringens enterotoxin
  • CPE-R, C perfringens enterotoxin receptor
  • CFTR, cystic fibrosis transmembrane conductance regulator
  • CaCC, calcium activated chloride channel
  • GC-C, guanylate cyclase C
  • ST, stable toxins
  • DAG, diacylglycerol
  • IP3, inositol 1,4,5-trisphosphate
  • TDH, thermostable direct haemolysin
  • Gal-1R, galanin-1 receptor
  • LPS, lipopolysaccharide
  • NO, nitric oxide
  • NOS, nitric oxide synthase
  • iNOS, inducible NOS
  • EIEC, enteroinvasive E coli
  • PGE2
  • prostaglandin E2
  • PGHS, prostaglandin H synthase
  • COX-2, cyclooxygenase 2
  • TLR, toll-like receptor
  • MHC, major histocompatibility complex
  • IL, interleukin
  • PEEC, pathogen elicited epithelial derived chemoattractant
  • NFκB, nuclear factor κB
  • TNF-α, tumour necrosis factor α
  • IκB, inhibitory protein κB
  • IKK, IκB kinase
  • NIK, NFκB inducing kinase
  • MAP, mitogen activated protein
  • MAPK, MAP kinase
  • MAPKKK, MAPK kinase kinase
  • MEK, MAP/ERK kinases
  • JNK, c-Jun NH2 terminal kinase
  • AP-1, activating protein 1
  • cag
  • cytotoxin associated antigen

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.