Microbiome, innate immunity, and esophageal adenocarcinoma

Clin Lab Med. 2014 Dec;34(4):721-32. doi: 10.1016/j.cll.2014.08.001. Epub 2014 Sep 26.


With the development of culture-independent technique, a complex microbiome has been established and described in the distal esophagus. The incidence of esophageal adenocarcinoma (EAC) has increased dramatically in the United States. Studies documenting an altered microbiome associated with EAC and its precedents suggest that dysbiosis may be contributing to carcinogenesis, potentially mediated by interactions with toll-like receptors. Investigations attempting to associate viruses with EAC have not been as consistent. Currently available data are cross-sectional and therefore cannot prove causal relationships. Prospectively, microbiome studies open a new avenue to the understanding of the etiology and pathogenesis of reflux disorders and EAC.

Keywords: Adenocarcinoma; Bacteria; Barrett esophagus; Chronic inflammation; Innate immunity; Microbiome; Reflux; Viruses.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Adenocarcinoma / immunology
  • Adenocarcinoma / microbiology*
  • Adenocarcinoma / virology
  • Alphapapillomavirus / pathogenicity
  • Barrett Esophagus / microbiology
  • Esophageal Neoplasms / immunology
  • Esophageal Neoplasms / microbiology*
  • Esophageal Neoplasms / virology
  • Esophagus / microbiology
  • Humans
  • Immunity, Innate*
  • Microbiota*
  • Toll-Like Receptors / metabolism
  • Toll-Like Receptors / physiology


  • Toll-Like Receptors