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

Alon Lang; Maor Lahav; Emad Sakhnini; Iris Barshack; Herma H. Fidder; Benjamin Avidan; Eitan Bardan; Rami Hershkoviz; Simon Bar-Meir; Yehuda Chowers

doi:10.1016/j.clnu.2004.03.011

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

Alon Lang, Maor Lahav, Emad Sakhnini, Iris Barshack, Herma H. Fidder, Benjamin Avidan, Eitan Bardan, Rami Hershkoviz, Simon Bar-Meir, Yehuda Chowers^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › Academic › peer-review

74 Citations (Scopus)

Abstract

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-α-stimulated secretion of IL-1β, 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-α-induced secretion of IL-1β, 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-1β mRNA levels. In addition, allicin suppressed the degradation of I κ B. 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.

Original language	English
Pages (from-to)	1199-1208
Number of pages	10
Journal	Clinical Nutrition
Volume	23
Issue number	5
DOIs	https://doi.org/10.1016/j.clnu.2004.03.011
Publication status	Published - Oct 2004

Keywords

Allicin
Chemokines
Cytokines
Epithelial cells
Intestine
TNF-α

Access to Document

10.1016/j.clnu.2004.03.011

Cite this

@article{0a2c9c551eda485f83310eb5ce467511,

title = "Allicin inhibits spontaneous and TNF-α induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells",

abstract = "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-α-stimulated secretion of IL-1β, 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-α-induced secretion of IL-1β, 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-1β mRNA levels. In addition, allicin suppressed the degradation of I κ B. 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.",

keywords = "Allicin, Chemokines, Cytokines, Epithelial cells, Intestine, TNF-α",

author = "Alon Lang and Maor Lahav and Emad Sakhnini and Iris Barshack and Fidder, {Herma H.} and Benjamin Avidan and Eitan Bardan and Rami Hershkoviz and Simon Bar-Meir and Yehuda Chowers",

year = "2004",

month = oct,

doi = "10.1016/j.clnu.2004.03.011",

language = "English",

volume = "23",

pages = "1199--1208",

journal = "Clinical Nutrition",

issn = "0261-5614",

publisher = "Churchill Livingstone",

number = "5",

}

TY - JOUR

T1 - Allicin inhibits spontaneous and TNF-α induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells

AU - Lang, Alon

AU - Lahav, Maor

AU - Sakhnini, Emad

AU - Barshack, Iris

AU - Fidder, Herma H.

AU - Avidan, Benjamin

AU - Bardan, Eitan

AU - Hershkoviz, Rami

AU - Bar-Meir, Simon

AU - Chowers, Yehuda

PY - 2004/10

Y1 - 2004/10

N2 - 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-α-stimulated secretion of IL-1β, 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-α-induced secretion of IL-1β, 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-1β mRNA levels. In addition, allicin suppressed the degradation of I κ B. 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.

AB - 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-α-stimulated secretion of IL-1β, 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-α-induced secretion of IL-1β, 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-1β mRNA levels. In addition, allicin suppressed the degradation of I κ B. 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.

KW - Allicin

KW - Chemokines

KW - Cytokines

KW - Epithelial cells

KW - Intestine

KW - TNF-α

UR - http://www.scopus.com/inward/record.url?scp=4544226878&partnerID=8YFLogxK

U2 - 10.1016/j.clnu.2004.03.011

DO - 10.1016/j.clnu.2004.03.011

M3 - Article

C2 - 15380914

AN - SCOPUS:4544226878

SN - 0261-5614

VL - 23

SP - 1199

EP - 1208

JO - Clinical Nutrition

JF - Clinical Nutrition

IS - 5

ER -

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

Abstract

Keywords

Access to Document

Other files and links

Fingerprint

Cite this