Vancomycin-resistant enterococci exploit antibiotic-induced innate immune deficits Academic Article uri icon


MeSH Major

  • Enterococcus
  • Immunity, Innate
  • Vancomycin
  • Vancomycin Resistance


  • Infection with antibiotic-resistant bacteria, such as vancomycin-resistant Enterococcus (VRE), is a dangerous and costly complication of broad-spectrum antibiotic therapy. How antibiotic-mediated elimination of commensal bacteria promotes infection by antibiotic-resistant bacteria is a fertile area for speculation with few defined mechanisms. Here we demonstrate that antibiotic treatment of mice notably downregulates intestinal expression of RegIIIgamma (also known as Reg3g), a secreted C-type lectin that kills Gram-positive bacteria, including VRE. Downregulation of RegIIIgamma markedly decreases in vivo killing of VRE in the intestine of antibiotic-treated mice. Stimulation of intestinal Toll-like receptor 4 by oral administration of lipopolysaccharide re-induces RegIIIgamma, thereby boosting innate immune resistance of antibiotic-treated mice against VRE. Compromised mucosal innate immune defence, as induced by broad-spectrum antibiotic therapy, can be corrected by selectively stimulating mucosal epithelial Toll-like receptors, providing a potential therapeutic approach to reduce colonization and infection by antibiotic-resistant microbes.

publication date

  • October 9, 2008



  • Academic Article



  • eng

PubMed Central ID

  • PMC2663337

Digital Object Identifier (DOI)

  • 10.1038/nature07250

PubMed ID

  • 18724361

Additional Document Info

start page

  • 804

end page

  • 7


  • 455


  • 7214