Microbial patterns signaling via Toll-like receptors 2 and 5 contribute to epithelial repair, growth and survival. Academic Article uri icon

Overview

MeSH

  • Cells, Cultured
  • Epithelium
  • Humans
  • Ligands

MeSH Major

  • Signal Transduction
  • Staphylococcus aureus
  • Toll-Like Receptor 2
  • Toll-Like Receptor 5
  • Wound Healing

abstract

  • Epithelial cells (ECs) continuously interact with microorganisms and detect their presence via different pattern-recognition receptors (PRRs) including Toll-like receptors (TLRs). Ligation of epithelial TLRs by pathogens is usually associated with the induction of pro-inflammatory mediators and antimicrobial factors. In this study, using human airway ECs as a model, we found that detection of microbial patterns via epithelial TLRs directly regulates tissue homeostasis. Staphylococcus aureus (S. aureus) and microbial patterns signaling via TLR2 and TLR5 induce a set of non-immune epithelial responses including cell migration, wound repair, proliferation, and survival of primary and cancerous ECs. Using small interfering RNA (siRNA) gene targeting, receptor-tyrosine kinase microarray and inhibition studies, we determined that TLR and the epidermal growth factor receptor (EGFR) mediate the stimulating effect of microbial patterns on epithelial repair. Microbial patterns signaling via Toll-like receptors 2 and 5 contribute to epithelial repair, growth and survival. This effect is independent of hematopoietic and other cells as well as inflammatory cytokines suggesting that epithelia are able to regulate their integrity in an autonomous non-inflammatory manner by sensing microbes directly via TLRs.

publication date

  • January 2, 2008

has subject area

  • Cells, Cultured
  • Epithelium
  • Humans
  • Ligands
  • Signal Transduction
  • Staphylococcus aureus
  • Toll-Like Receptor 2
  • Toll-Like Receptor 5
  • Wound Healing

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2148109

Digital Object Identifier (DOI)

  • 10.1371/journal.pone.0001393

PubMed ID

  • 18167552

Additional Document Info

start page

  • e1393

volume

  • 3

number

  • 1