Allicin inhibits spontaneous and TNF-α induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells
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 al...
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| Veröffentlicht in: | Clinical nutrition (Edinburgh, Scotland) Scotland), 2004-10, Vol.23 (5), p.1199-1208 |
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| container_title | Clinical nutrition (Edinburgh, Scotland) |
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| creator | Lang, Alon Lahav, Maor Sakhnini, Emad Barshack, Iris Fidder, Herma H. Avidan, Benjamin Bardan, Eitan Hershkoviz, Rami Bar-Meir, Simon Chowers, Yehuda |
| description | 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
κB. 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. |
| doi_str_mv | 10.1016/j.clnu.2004.03.011 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_66898651</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0261561404000585</els_id><sourcerecordid>66898651</sourcerecordid><originalsourceid>FETCH-LOGICAL-e290t-43be0a4e004436c0b1aa85516e49ae510ebb8f8c0e088dbfc469da50379b2a8a3</originalsourceid><addsrcrecordid>eNpFkU1u1DAUxy0EotPCBVggb2CX9DmOXUdiU1WUIlVlU9aW47xoPDj2EDuV5gK9Ty_CmXA0g1jZ1vv56f9ByAcGNQMmL3e19WGpG4C2Bl4DY6_IhgneVKxT_DXZQCNZJSRrz8h5SjsAEPxKvSVnBVLQsXZDnq-9d9YF6sLW9S4nmvYxZBMwLomaMNDHh9vqz0uZD4vFgSa0M2YXA40j3c_RhdGbaTI5zgdqDzn-cgGPP-0Wp9NznONUVmRM2QXjKe5d3qJ35WrR-_SOvBmNT_j-dF6Qn7dfH2_uqvsf377fXN9X2HSQq5b3CKbF4rjl0kLPjFFCMIltZ1AwwL5Xo7KAoNTQj7aV3WAE8Kuub4wy_IJ8Pu4tyn8vRY2eXFoVHA1rKVWnpGAF_HgCl37CQe9nN5n5oP8lV4BPJ8Aka_w4m2Bd-s-V1JkUK_flyGGx9eRw1sk6DCVKN6PNeohOM9BroXqn10L1WqgGrkuh_C9UoZbH</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>66898651</pqid></control><display><type>article</type><title>Allicin inhibits spontaneous and TNF-α induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Lang, Alon ; Lahav, Maor ; Sakhnini, Emad ; Barshack, Iris ; Fidder, Herma H. ; Avidan, Benjamin ; Bardan, Eitan ; Hershkoviz, Rami ; Bar-Meir, Simon ; Chowers, Yehuda</creator><creatorcontrib>Lang, Alon ; Lahav, Maor ; Sakhnini, Emad ; Barshack, Iris ; Fidder, Herma H. ; Avidan, Benjamin ; Bardan, Eitan ; Hershkoviz, Rami ; Bar-Meir, Simon ; Chowers, Yehuda</creatorcontrib><description>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
κB. 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.</description><identifier>ISSN: 0261-5614</identifier><identifier>EISSN: 1532-1983</identifier><identifier>DOI: 10.1016/j.clnu.2004.03.011</identifier><identifier>PMID: 15380914</identifier><identifier>CODEN: CLNUDP</identifier><language>eng</language><publisher>Kidlington: Elsevier Ltd</publisher><subject>Allicin ; Anti-Infective Agents - pharmacology ; Biological and medical sciences ; Caco-2 Cells ; Chemokine CXCL10 - antagonists & inhibitors ; Chemokine CXCL10 - secretion ; Chemokines ; Cytokines ; Dose-Response Relationship, Immunologic ; Epithelial cells ; Feeding. Feeding behavior ; Fundamental and applied biological sciences. Psychology ; HT29 Cells ; Humans ; Immunosuppressive Agents - pharmacology ; Interleukin-1 - antagonists & inhibitors ; Interleukin-1 - secretion ; Interleukin-8 - antagonists & inhibitors ; Interleukin-8 - secretion ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - immunology ; Intestinal Mucosa - secretion ; Intestine ; RNA, Messenger - metabolism ; Sulfinic Acids - pharmacology ; TNF-α ; Tumor Necrosis Factor-alpha - physiology ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>Clinical nutrition (Edinburgh, Scotland), 2004-10, Vol.23 (5), p.1199-1208</ispartof><rights>2004 Elsevier Ltd</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.clnu.2004.03.011$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16141654$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15380914$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lang, Alon</creatorcontrib><creatorcontrib>Lahav, Maor</creatorcontrib><creatorcontrib>Sakhnini, Emad</creatorcontrib><creatorcontrib>Barshack, Iris</creatorcontrib><creatorcontrib>Fidder, Herma H.</creatorcontrib><creatorcontrib>Avidan, Benjamin</creatorcontrib><creatorcontrib>Bardan, Eitan</creatorcontrib><creatorcontrib>Hershkoviz, Rami</creatorcontrib><creatorcontrib>Bar-Meir, Simon</creatorcontrib><creatorcontrib>Chowers, Yehuda</creatorcontrib><title>Allicin inhibits spontaneous and TNF-α induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells</title><title>Clinical nutrition (Edinburgh, Scotland)</title><addtitle>Clin Nutr</addtitle><description>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
κB. 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.</description><subject>Allicin</subject><subject>Anti-Infective Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Caco-2 Cells</subject><subject>Chemokine CXCL10 - antagonists & inhibitors</subject><subject>Chemokine CXCL10 - secretion</subject><subject>Chemokines</subject><subject>Cytokines</subject><subject>Dose-Response Relationship, Immunologic</subject><subject>Epithelial cells</subject><subject>Feeding. Feeding behavior</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Interleukin-1 - antagonists & inhibitors</subject><subject>Interleukin-1 - secretion</subject><subject>Interleukin-8 - antagonists & inhibitors</subject><subject>Interleukin-8 - secretion</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Intestinal Mucosa - immunology</subject><subject>Intestinal Mucosa - secretion</subject><subject>Intestine</subject><subject>RNA, Messenger - metabolism</subject><subject>Sulfinic Acids - pharmacology</subject><subject>TNF-α</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>0261-5614</issn><issn>1532-1983</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkU1u1DAUxy0EotPCBVggb2CX9DmOXUdiU1WUIlVlU9aW47xoPDj2EDuV5gK9Ty_CmXA0g1jZ1vv56f9ByAcGNQMmL3e19WGpG4C2Bl4DY6_IhgneVKxT_DXZQCNZJSRrz8h5SjsAEPxKvSVnBVLQsXZDnq-9d9YF6sLW9S4nmvYxZBMwLomaMNDHh9vqz0uZD4vFgSa0M2YXA40j3c_RhdGbaTI5zgdqDzn-cgGPP-0Wp9NznONUVmRM2QXjKe5d3qJ35WrR-_SOvBmNT_j-dF6Qn7dfH2_uqvsf377fXN9X2HSQq5b3CKbF4rjl0kLPjFFCMIltZ1AwwL5Xo7KAoNTQj7aV3WAE8Kuub4wy_IJ8Pu4tyn8vRY2eXFoVHA1rKVWnpGAF_HgCl37CQe9nN5n5oP8lV4BPJ8Aka_w4m2Bd-s-V1JkUK_flyGGx9eRw1sk6DCVKN6PNeohOM9BroXqn10L1WqgGrkuh_C9UoZbH</recordid><startdate>20041001</startdate><enddate>20041001</enddate><creator>Lang, Alon</creator><creator>Lahav, Maor</creator><creator>Sakhnini, Emad</creator><creator>Barshack, Iris</creator><creator>Fidder, Herma H.</creator><creator>Avidan, Benjamin</creator><creator>Bardan, Eitan</creator><creator>Hershkoviz, Rami</creator><creator>Bar-Meir, Simon</creator><creator>Chowers, Yehuda</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20041001</creationdate><title>Allicin inhibits spontaneous and TNF-α induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells</title><author>Lang, Alon ; Lahav, Maor ; Sakhnini, Emad ; Barshack, Iris ; Fidder, Herma H. ; Avidan, Benjamin ; Bardan, Eitan ; Hershkoviz, Rami ; Bar-Meir, Simon ; Chowers, Yehuda</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e290t-43be0a4e004436c0b1aa85516e49ae510ebb8f8c0e088dbfc469da50379b2a8a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Allicin</topic><topic>Anti-Infective Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Caco-2 Cells</topic><topic>Chemokine CXCL10 - antagonists & inhibitors</topic><topic>Chemokine CXCL10 - secretion</topic><topic>Chemokines</topic><topic>Cytokines</topic><topic>Dose-Response Relationship, Immunologic</topic><topic>Epithelial cells</topic><topic>Feeding. Feeding behavior</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>HT29 Cells</topic><topic>Humans</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Interleukin-1 - antagonists & inhibitors</topic><topic>Interleukin-1 - secretion</topic><topic>Interleukin-8 - antagonists & inhibitors</topic><topic>Interleukin-8 - secretion</topic><topic>Intestinal Mucosa - drug effects</topic><topic>Intestinal Mucosa - immunology</topic><topic>Intestinal Mucosa - secretion</topic><topic>Intestine</topic><topic>RNA, Messenger - metabolism</topic><topic>Sulfinic Acids - pharmacology</topic><topic>TNF-α</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lang, Alon</creatorcontrib><creatorcontrib>Lahav, Maor</creatorcontrib><creatorcontrib>Sakhnini, Emad</creatorcontrib><creatorcontrib>Barshack, Iris</creatorcontrib><creatorcontrib>Fidder, Herma H.</creatorcontrib><creatorcontrib>Avidan, Benjamin</creatorcontrib><creatorcontrib>Bardan, Eitan</creatorcontrib><creatorcontrib>Hershkoviz, Rami</creatorcontrib><creatorcontrib>Bar-Meir, Simon</creatorcontrib><creatorcontrib>Chowers, Yehuda</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical nutrition (Edinburgh, Scotland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lang, Alon</au><au>Lahav, Maor</au><au>Sakhnini, Emad</au><au>Barshack, Iris</au><au>Fidder, Herma H.</au><au>Avidan, Benjamin</au><au>Bardan, Eitan</au><au>Hershkoviz, Rami</au><au>Bar-Meir, Simon</au><au>Chowers, Yehuda</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Allicin inhibits spontaneous and TNF-α induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells</atitle><jtitle>Clinical nutrition (Edinburgh, Scotland)</jtitle><addtitle>Clin Nutr</addtitle><date>2004-10-01</date><risdate>2004</risdate><volume>23</volume><issue>5</issue><spage>1199</spage><epage>1208</epage><pages>1199-1208</pages><issn>0261-5614</issn><eissn>1532-1983</eissn><coden>CLNUDP</coden><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
κB. 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.</abstract><cop>Kidlington</cop><pub>Elsevier Ltd</pub><pmid>15380914</pmid><doi>10.1016/j.clnu.2004.03.011</doi><tpages>10</tpages></addata></record> |
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| ispartof | Clinical nutrition (Edinburgh, Scotland), 2004-10, Vol.23 (5), p.1199-1208 |
| issn | 0261-5614 1532-1983 |
| language | eng |
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| subjects | Allicin Anti-Infective Agents - pharmacology Biological and medical sciences Caco-2 Cells Chemokine CXCL10 - antagonists & inhibitors Chemokine CXCL10 - secretion Chemokines Cytokines Dose-Response Relationship, Immunologic Epithelial cells Feeding. Feeding behavior Fundamental and applied biological sciences. Psychology HT29 Cells Humans Immunosuppressive Agents - pharmacology Interleukin-1 - antagonists & inhibitors Interleukin-1 - secretion Interleukin-8 - antagonists & inhibitors Interleukin-8 - secretion Intestinal Mucosa - drug effects Intestinal Mucosa - immunology Intestinal Mucosa - secretion Intestine RNA, Messenger - metabolism Sulfinic Acids - pharmacology TNF-α Tumor Necrosis Factor-alpha - physiology Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | Allicin inhibits spontaneous and TNF-α induced secretion of proinflammatory cytokines and chemokines from intestinal epithelial cells |
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