title: Allicin inhibits spontaneous and TNF-alpha induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells.
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Gastroenterology, Chaim Sheba Medical Center, Affiliaated to the Tel-Aviv University, Tel-Hashomer 5261, Israel.
authors.forename: Alon
authors.initials: A
authors.lastname: Lang
authors.forename: Maor
authors.initials: M
authors.lastname: Lahav
authors.forename: Emad
authors.initials: E
authors.lastname: Sakhnini
authors.forename: Iris
authors.initials: I
authors.lastname: Barshack
authors.forename: Herma H
authors.initials: HH
authors.lastname: Fidder
authors.forename: Benjamin
authors.initials: B
authors.lastname: Avidan
authors.forename: Eitan
authors.initials: E
authors.lastname: Bardan
authors.forename: Rami
authors.initials: R
authors.lastname: Hershkoviz
authors.forename: Simon
authors.initials: S
authors.lastname: Bar-Meir
authors.forename: Yehuda
authors.initials: Y
authors.lastname: Chowers
mesh_terms: D000890:Anti-Infective Agents / Q000494:pharmacology*; D018938:Caco-2 Cells; D054357:Chemokine CXCL10 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D004220:Disulfides; D004306:Dose-Response Relationship, Immunologic; D019073:HT29 Cells; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D007375:Interleukin-1 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D016209:Interleukin-8 / Q000037:antagonists & inhibitors* / Q000378:metabolism; D007413:Intestinal Mucosa / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D013441:Sulfinic Acids / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
chemical_list: D000890:Anti-Infective Agents; D054357:Chemokine CXCL10; D004220:Disulfides; D007166:Immunosuppressive Agents; D007375:Interleukin-1; D016209:Interleukin-8; D012333:RNA, Messenger; D013441:Sulfinic Acids; D014409:Tumor Necrosis Factor-alpha; C006452:allicin