Methionine deficiency reduces autophagy and accelerates death in intestinal epithelial cells infected with enterotoxigenic Escherichia coli

Amino Acids. 2015 Oct;47(10):2199-204. doi: 10.1007/s00726-014-1781-4. Epub 2014 Jun 26.

Abstract

Infections by enterotoxigenic Escherichia coli (ETEC) result in large economic losses to the swine industry worldwide. Dietary supplementation with amino acids has been considered as a potential mechanism to improve host defenses against infection. The goal of this study was to determine whether methionine deprivation alters ETEC interactions with porcine intestinal epithelial cells. IPEC-1 cells were cultured in media with or without L-methionine. Methionine deprivation resulted in enhanced ETEC adhesion and increased both the cytotoxicity and apoptotic responses of IPEC-1 cells infected with ETEC. Methionine deprivation inhibited IPEC-1 cell autophagic responses, suggesting that the increased cytotoxicity of ETEC to methionine-deprived IPEC-1 cells might be due to defects in autophagy.

Keywords: Apoptosis; Autophagy; Cytotoxicity; Enterotoxigenic Escherichia coli; IPEC-1; Methionine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects
  • Autophagy*
  • Bacterial Adhesion / drug effects
  • Blotting, Western
  • Cell Proliferation / drug effects
  • Cells, Cultured
  • Enterotoxigenic Escherichia coli / pathogenicity*
  • Epithelial Cells / drug effects
  • Epithelial Cells / microbiology
  • Epithelial Cells / pathology*
  • Escherichia coli Infections / microbiology*
  • Intestines / drug effects
  • Intestines / microbiology
  • Intestines / pathology*
  • Methionine / deficiency*
  • Methionine / pharmacology
  • Signal Transduction / drug effects
  • Swine

Substances

  • Methionine