Allicin inhibits spontaneous and TNF-alpha induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells

Clin Nutr. 2004 Oct;23(5):1199-208. doi: 10.1016/j.clnu.2004.03.011.


Background & aims: Allicin, the active substance of fresh crushed garlic has different biological activities and was implicated as an anti-inflammatory agent. Epithelial cells have an important role in intestinal inflammation. The aim of this study was to assess the immunomodulatory effect of allicin on intestinal epithelial cells.

Methods: The spontaneous and TNF-alpha-stimulated secretion of IL-1beta, IL-8, IP-10 and MIG from HT-29 and Caco-2 cells was tested with, or without pretreatment with allicin. Cytokine secretion was assessed using ELISA and expression of mRNA was determined by an RNA protection assay.

Results: Allicin markedly inhibited the spontaneous and TNF-alpha -induced secretion of IL-1beta, IL-8, IP-10 and MIG from the two different cell lines in a dose-dependent manner and suppressed the expression of IL-8 and IL-1beta mRNA levels. In addition, allicin suppressed the degradation of IkappaB. No effect on cell viability was noted.

Conclusions: These observations indicate that allicin exerts an inhibitory immunomodulatory effect on intestinal epithelial cells and suggest that allicin may have the potential to attenuate intestinal inflammation.

MeSH terms

  • Anti-Infective Agents / pharmacology*
  • Caco-2 Cells
  • Chemokine CXCL10 / antagonists & inhibitors*
  • Chemokine CXCL10 / metabolism
  • Disulfides
  • Dose-Response Relationship, Immunologic
  • HT29 Cells
  • Humans
  • Immunosuppressive Agents / pharmacology*
  • Interleukin-1 / antagonists & inhibitors*
  • Interleukin-1 / metabolism
  • Interleukin-8 / antagonists & inhibitors*
  • Interleukin-8 / metabolism
  • Intestinal Mucosa / drug effects
  • Intestinal Mucosa / immunology
  • Intestinal Mucosa / metabolism
  • RNA, Messenger / metabolism
  • Sulfinic Acids / pharmacology*
  • Tumor Necrosis Factor-alpha / physiology*


  • Anti-Infective Agents
  • Chemokine CXCL10
  • Disulfides
  • Immunosuppressive Agents
  • Interleukin-1
  • Interleukin-8
  • RNA, Messenger
  • Sulfinic Acids
  • Tumor Necrosis Factor-alpha
  • allicin