TLR2, TLR3, and TLR4 activation specifically alters the oxidative status of intestinal epithelial cells

Cell Stress Chaperones. 2014 Mar;19(2):289-93. doi: 10.1007/s12192-013-0461-8. Epub 2013 Sep 26.

Abstract

Intestinal inflammatory diseases are the result of multiple processes, including mucosal oxidative stress and perturbed homeostasis between commensal bacteria and mucosal immunity. Toll-like receptors (TLRs) recognize molecular-associated microorganisms' patterns and trigger innate immunity responses contributing to intestinal homeostasis and inflammatory responses. However, TLRs effects on redox balance in intestinal mucosa remain unknown. Therefore, the present study analyzes the effect of TLR2, TLR3, and TLR4 on both oxidative damage of lipids and proteins, and the activity of antioxidant enzymes in enterocyte-like Caco-2 cells. The results show that the activation of these TLRs increased lipid and protein oxidation levels; however, the effect on the antioxidant enzymes activity is different depending on the TLR activated. These results suggest that the activation of TLR2, TLR3, and TLR4 might affect intestinal inflammation by not only their inherent innate immunity responses, but also their pro-oxidative effects on intestinal epithelial cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Caco-2 Cells
  • Catalase / metabolism
  • Epithelial Cells / metabolism*
  • Glutathione Peroxidase / metabolism
  • Humans
  • Intestinal Mucosa / cytology*
  • Lipid Peroxidation
  • Oxidation-Reduction
  • Superoxide Dismutase / metabolism
  • Toll-Like Receptor 2 / metabolism
  • Toll-Like Receptor 3 / metabolism
  • Toll-Like Receptor 4 / metabolism
  • Toll-Like Receptors / metabolism*

Substances

  • TLR2 protein, human
  • TLR3 protein, human
  • TLR4 protein, human
  • Toll-Like Receptor 2
  • Toll-Like Receptor 3
  • Toll-Like Receptor 4
  • Toll-Like Receptors
  • Catalase
  • Glutathione Peroxidase
  • Superoxide Dismutase