Entamoeba histolytica stimulates interleukin 8 from human colonic epithelial cells without parasite-enterocyte contact

Gastroenterology. 1997 May;112(5):1536-47. doi: 10.1016/s0016-5085(97)70035-0.


Background & aims: The mechanisms involved in the initiation of host mucosal inflammation in amebiasis are not fully understood. This study characterized the effect of Entamoeba histolytica components on interleukin 8 (IL-8) gene expression in human colonic cells.

Methods: Colonic cells were stimulated with amebic proteins, secretory components, or live trophozoites (separated with 0.45-microm pores), and the levels of IL-8 messenger RNA (mRNA) and protein were detected.

Results: Live amebae or their components enhanced IL-8 mRNA levels in the colonic cells (T84, LS174T, and Caco-2). In T84 cells, the accumulation of IL-8 mRNA induced by amebic components occurred in a dose- and time-dependent fashion. Increased secretion of IL-8 was noted after 12-hour stimulation; neutralizing antibodies against IL-15 or tumor necrosis factor alpha did not inhibit IL-8 production. Nuclear run-on assays showed that amebae-induced IL-8 gene occurred by a posttranscriptional mechanism. Cycloheximide treatment resulted in superinduction of IL-8 mRNA; however, dexamethasone inhibited E. histolytica-induced IL-8 gene expression.

Conclusions: E. histolytica can directly stimulate the induction of IL-8 by colonic cells in the absence of cell-cell contact or injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Communication*
  • Cell Line
  • Colon / cytology
  • Colon / metabolism*
  • Cycloheximide / pharmacology
  • Dexamethasone / pharmacology
  • Entamoeba histolytica / metabolism
  • Entamoeba histolytica / physiology*
  • Glucocorticoids / pharmacology
  • Host-Parasite Interactions*
  • Humans
  • Interleukin-1 / physiology
  • Interleukin-8 / genetics
  • Interleukin-8 / metabolism*
  • Intestinal Mucosa / cytology
  • Intestinal Mucosa / metabolism*
  • Protein Synthesis Inhibitors / pharmacology
  • RNA, Messenger / metabolism
  • Time Factors
  • Tumor Necrosis Factor-alpha / physiology


  • Glucocorticoids
  • Interleukin-1
  • Interleukin-8
  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Dexamethasone
  • Cycloheximide