Sirolimus ameliorates inflammatory responses by switching the regulatory T/T helper type 17 profile in murine colitis.
Identifieur interne : 000F82 ( Main/Exploration ); précédent : 000F81; suivant : 000F83Sirolimus ameliorates inflammatory responses by switching the regulatory T/T helper type 17 profile in murine colitis.
Auteurs : Hui Yin [République populaire de Chine] ; Xiangyong Li ; Bobin Zhang ; Tao Liu ; Baohong Yuan ; Qian Ni ; Shilian Hu ; Hongbiao GuSource :
- Immunology [ 1365-2567 ] ; 2013.
Descripteurs français
- KwdFr :
- Acide 2,4,6-trinitro-benzènesulfonique (MeSH), Animaux (MeSH), Anti-inflammatoires (administration et posologie), Anti-inflammatoires (pharmacologie), Cellules Th17 (effets des médicaments et des substances chimiques), Cellules Th17 (immunologie), Cellules cultivées (MeSH), Colite (anatomopathologie), Colite (immunologie), Colite (induit chimiquement), Colite (prévention et contrôle), Côlon (anatomopathologie), Côlon (effets des médicaments et des substances chimiques), Côlon (immunologie), Facteur de croissance transformant bêta (métabolisme), Facteur de nécrose tumorale alpha (métabolisme), Facteurs de transcription Forkhead (métabolisme), Facteurs temps (MeSH), Immunosuppresseurs (administration et posologie), Immunosuppresseurs (pharmacologie), Injections péritoneales (MeSH), Interleukine-17 (métabolisme), Interleukine-6 (métabolisme), Modèles animaux de maladie humaine (MeSH), Mâle (MeSH), Médiateurs de l'inflammation (métabolisme), Noeuds lymphatiques (effets des médicaments et des substances chimiques), Noeuds lymphatiques (immunologie), Numération des lymphocytes CD4 (MeSH), Phénotype (MeSH), Sirolimus (administration et posologie), Sirolimus (pharmacologie), Souris (MeSH), Souris de lignée BALB C (MeSH).
- MESH :
- administration et posologie : Anti-inflammatoires, Immunosuppresseurs, Sirolimus.
- anatomopathologie : Colite, Côlon.
- effets des médicaments et des substances chimiques : Cellules Th17, Côlon, Noeuds lymphatiques.
- immunologie : Cellules Th17, Colite, Côlon, Noeuds lymphatiques.
- induit chimiquement : Colite.
- métabolisme : Facteur de croissance transformant bêta, Facteur de nécrose tumorale alpha, Facteurs de transcription Forkhead, Interleukine-17, Interleukine-6, Médiateurs de l'inflammation.
- pharmacologie : Anti-inflammatoires, Immunosuppresseurs, Sirolimus.
- prévention et contrôle : Colite.
- Acide 2,4,6-trinitro-benzènesulfonique, Animaux, Cellules cultivées, Facteurs temps, Injections péritoneales, Modèles animaux de maladie humaine, Mâle, Numération des lymphocytes CD4, Phénotype, Souris, Souris de lignée BALB C.
English descriptors
- KwdEn :
- Animals (MeSH), Anti-Inflammatory Agents (administration & dosage), Anti-Inflammatory Agents (pharmacology), CD4 Lymphocyte Count (MeSH), Cells, Cultured (MeSH), Colitis (chemically induced), Colitis (immunology), Colitis (pathology), Colitis (prevention & control), Colon (drug effects), Colon (immunology), Colon (pathology), Disease Models, Animal (MeSH), Forkhead Transcription Factors (metabolism), Immunosuppressive Agents (administration & dosage), Immunosuppressive Agents (pharmacology), Inflammation Mediators (metabolism), Injections, Intraperitoneal (MeSH), Interleukin-17 (metabolism), Interleukin-6 (metabolism), Lymph Nodes (drug effects), Lymph Nodes (immunology), Male (MeSH), Mice (MeSH), Mice, Inbred BALB C (MeSH), Phenotype (MeSH), Sirolimus (administration & dosage), Sirolimus (pharmacology), Th17 Cells (drug effects), Th17 Cells (immunology), Time Factors (MeSH), Transforming Growth Factor beta (metabolism), Trinitrobenzenesulfonic Acid (MeSH), Tumor Necrosis Factor-alpha (metabolism).
- MESH :
- chemical , administration & dosage : Anti-Inflammatory Agents, Immunosuppressive Agents, Sirolimus.
- chemical , metabolism : Forkhead Transcription Factors, Inflammation Mediators, Interleukin-17, Interleukin-6, Transforming Growth Factor beta, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Anti-Inflammatory Agents, Immunosuppressive Agents, Sirolimus.
- chemically induced : Colitis.
- drug effects : Colon, Lymph Nodes, Th17 Cells.
- immunology : Colitis, Colon, Lymph Nodes, Th17 Cells.
- pathology : Colitis, Colon.
- prevention & control : Colitis.
- Animals, CD4 Lymphocyte Count, Cells, Cultured, Disease Models, Animal, Injections, Intraperitoneal, Male, Mice, Mice, Inbred BALB C, Phenotype, Time Factors, Trinitrobenzenesulfonic Acid.
Abstract
Inflammatory bowel disease is characterized by dysregulated immune responses in inflamed intestine, with dominance of interleukin-17 (IL-17)--producing cells and deficiency of regulatory T (Treg) cells. The aim of this study was to investigate the effect and mechanisms of sirolimus, an inhibitor of the mammalian target of rapamycin, on immune responses in a murine model of Crohn's disease. Murine colitis was induced by intrarectal administration of 2,4,6-trinitrobenzene sulphonic acid at day 0. Mice were then treated intraperitoneally with sirolimus daily for 3 days. The gross and histological appearances of the colon and the numbers, phenotype and cytokine production of lymphocytes were compared with these characteristics in a control group. Sirolimus treatment significantly decreased all macroscopic, microscopic and histopathological parameters of colitis that were analysed. The therapeutic effects of sirolimus were associated with a down-regulation of pro-inflammatory cytokines tumour necrosis factor-α, IL-6 and IL-17A. Intriguingly, sirolimus administration resulted in a prominent up-regulation of the regulatory cytokine transforming growth factor-β. Supporting the hypothesis that sirolimus directly affects the functional activity of CD4+ CD25+ Treg cells, we observed a remarkable enhancement of FoxP3 expression in colon tissues and isolated CD4+ T cells of sirolimus-treated mice. Simultaneously, sirolimus treatment led to a significant reduction in the number of CD4+ IL-17A+ T cells in the mesenteric lymph node cells as well as IL-17A production in mesenteric lymph node cells. Therefore, sirolimus may offer a promising new therapeutic strategy for the treatment of inflammatory bowel disease.
DOI: 10.1111/imm.12096
PubMed: 23480027
PubMed Central: PMC3719066
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Anti-Inflammatory Agents (administration & dosage)</term>
<term>Anti-Inflammatory Agents (pharmacology)</term>
<term>CD4 Lymphocyte Count (MeSH)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Colitis (chemically induced)</term>
<term>Colitis (immunology)</term>
<term>Colitis (pathology)</term>
<term>Colitis (prevention & control)</term>
<term>Colon (drug effects)</term>
<term>Colon (immunology)</term>
<term>Colon (pathology)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Forkhead Transcription Factors (metabolism)</term>
<term>Immunosuppressive Agents (administration & dosage)</term>
<term>Immunosuppressive Agents (pharmacology)</term>
<term>Inflammation Mediators (metabolism)</term>
<term>Injections, Intraperitoneal (MeSH)</term>
<term>Interleukin-17 (metabolism)</term>
<term>Interleukin-6 (metabolism)</term>
<term>Lymph Nodes (drug effects)</term>
<term>Lymph Nodes (immunology)</term>
<term>Male (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred BALB C (MeSH)</term>
<term>Phenotype (MeSH)</term>
<term>Sirolimus (administration & dosage)</term>
<term>Sirolimus (pharmacology)</term>
<term>Th17 Cells (drug effects)</term>
<term>Th17 Cells (immunology)</term>
<term>Time Factors (MeSH)</term>
<term>Transforming Growth Factor beta (metabolism)</term>
<term>Trinitrobenzenesulfonic Acid (MeSH)</term>
<term>Tumor Necrosis Factor-alpha (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Acide 2,4,6-trinitro-benzènesulfonique (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Anti-inflammatoires (administration et posologie)</term>
<term>Anti-inflammatoires (pharmacologie)</term>
<term>Cellules Th17 (effets des médicaments et des substances chimiques)</term>
<term>Cellules Th17 (immunologie)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Colite (anatomopathologie)</term>
<term>Colite (immunologie)</term>
<term>Colite (induit chimiquement)</term>
<term>Colite (prévention et contrôle)</term>
<term>Côlon (anatomopathologie)</term>
<term>Côlon (effets des médicaments et des substances chimiques)</term>
<term>Côlon (immunologie)</term>
<term>Facteur de croissance transformant bêta (métabolisme)</term>
<term>Facteur de nécrose tumorale alpha (métabolisme)</term>
<term>Facteurs de transcription Forkhead (métabolisme)</term>
<term>Facteurs temps (MeSH)</term>
<term>Immunosuppresseurs (administration et posologie)</term>
<term>Immunosuppresseurs (pharmacologie)</term>
<term>Injections péritoneales (MeSH)</term>
<term>Interleukine-17 (métabolisme)</term>
<term>Interleukine-6 (métabolisme)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Médiateurs de l'inflammation (métabolisme)</term>
<term>Noeuds lymphatiques (effets des médicaments et des substances chimiques)</term>
<term>Noeuds lymphatiques (immunologie)</term>
<term>Numération des lymphocytes CD4 (MeSH)</term>
<term>Phénotype (MeSH)</term>
<term>Sirolimus (administration et posologie)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée BALB C (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Immunosuppressive Agents</term>
<term>Sirolimus</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Forkhead Transcription Factors</term>
<term>Inflammation Mediators</term>
<term>Interleukin-17</term>
<term>Interleukin-6</term>
<term>Transforming Growth Factor beta</term>
<term>Tumor Necrosis Factor-alpha</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Immunosuppressive Agents</term>
<term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Anti-inflammatoires</term>
<term>Immunosuppresseurs</term>
<term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Colite</term>
<term>Côlon</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Colitis</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Colon</term>
<term>Lymph Nodes</term>
<term>Th17 Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Cellules Th17</term>
<term>Côlon</term>
<term>Noeuds lymphatiques</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules Th17</term>
<term>Colite</term>
<term>Côlon</term>
<term>Noeuds lymphatiques</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Colitis</term>
<term>Colon</term>
<term>Lymph Nodes</term>
<term>Th17 Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="induit chimiquement" xml:lang="fr"><term>Colite</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de croissance transformant bêta</term>
<term>Facteur de nécrose tumorale alpha</term>
<term>Facteurs de transcription Forkhead</term>
<term>Interleukine-17</term>
<term>Interleukine-6</term>
<term>Médiateurs de l'inflammation</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Colitis</term>
<term>Colon</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires</term>
<term>Immunosuppresseurs</term>
<term>Sirolimus</term>
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<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Colitis</term>
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<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Colite</term>
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<term>CD4 Lymphocyte Count</term>
<term>Cells, Cultured</term>
<term>Disease Models, Animal</term>
<term>Injections, Intraperitoneal</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Phenotype</term>
<term>Time Factors</term>
<term>Trinitrobenzenesulfonic Acid</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Acide 2,4,6-trinitro-benzènesulfonique</term>
<term>Animaux</term>
<term>Cellules cultivées</term>
<term>Facteurs temps</term>
<term>Injections péritoneales</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mâle</term>
<term>Numération des lymphocytes CD4</term>
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<term>Souris</term>
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<front><div type="abstract" xml:lang="en">Inflammatory bowel disease is characterized by dysregulated immune responses in inflamed intestine, with dominance of interleukin-17 (IL-17)--producing cells and deficiency of regulatory T (Treg) cells. The aim of this study was to investigate the effect and mechanisms of sirolimus, an inhibitor of the mammalian target of rapamycin, on immune responses in a murine model of Crohn's disease. Murine colitis was induced by intrarectal administration of 2,4,6-trinitrobenzene sulphonic acid at day 0. Mice were then treated intraperitoneally with sirolimus daily for 3 days. The gross and histological appearances of the colon and the numbers, phenotype and cytokine production of lymphocytes were compared with these characteristics in a control group. Sirolimus treatment significantly decreased all macroscopic, microscopic and histopathological parameters of colitis that were analysed. The therapeutic effects of sirolimus were associated with a down-regulation of pro-inflammatory cytokines tumour necrosis factor-α, IL-6 and IL-17A. Intriguingly, sirolimus administration resulted in a prominent up-regulation of the regulatory cytokine transforming growth factor-β. Supporting the hypothesis that sirolimus directly affects the functional activity of CD4+ CD25+ Treg cells, we observed a remarkable enhancement of FoxP3 expression in colon tissues and isolated CD4+ T cells of sirolimus-treated mice. Simultaneously, sirolimus treatment led to a significant reduction in the number of CD4+ IL-17A+ T cells in the mesenteric lymph node cells as well as IL-17A production in mesenteric lymph node cells. Therefore, sirolimus may offer a promising new therapeutic strategy for the treatment of inflammatory bowel disease.</div>
</front>
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<DateCompleted><Year>2013</Year>
<Month>09</Month>
<Day>09</Day>
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<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
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<JournalIssue CitedMedium="Internet"><Volume>139</Volume>
<Issue>4</Issue>
<PubDate><Year>2013</Year>
<Month>Aug</Month>
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<Title>Immunology</Title>
<ISOAbbreviation>Immunology</ISOAbbreviation>
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<ArticleTitle>Sirolimus ameliorates inflammatory responses by switching the regulatory T/T helper type 17 profile in murine colitis.</ArticleTitle>
<Pagination><MedlinePgn>494-502</MedlinePgn>
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<ELocationID EIdType="doi" ValidYN="Y">10.1111/imm.12096</ELocationID>
<Abstract><AbstractText>Inflammatory bowel disease is characterized by dysregulated immune responses in inflamed intestine, with dominance of interleukin-17 (IL-17)--producing cells and deficiency of regulatory T (Treg) cells. The aim of this study was to investigate the effect and mechanisms of sirolimus, an inhibitor of the mammalian target of rapamycin, on immune responses in a murine model of Crohn's disease. Murine colitis was induced by intrarectal administration of 2,4,6-trinitrobenzene sulphonic acid at day 0. Mice were then treated intraperitoneally with sirolimus daily for 3 days. The gross and histological appearances of the colon and the numbers, phenotype and cytokine production of lymphocytes were compared with these characteristics in a control group. Sirolimus treatment significantly decreased all macroscopic, microscopic and histopathological parameters of colitis that were analysed. The therapeutic effects of sirolimus were associated with a down-regulation of pro-inflammatory cytokines tumour necrosis factor-α, IL-6 and IL-17A. Intriguingly, sirolimus administration resulted in a prominent up-regulation of the regulatory cytokine transforming growth factor-β. Supporting the hypothesis that sirolimus directly affects the functional activity of CD4+ CD25+ Treg cells, we observed a remarkable enhancement of FoxP3 expression in colon tissues and isolated CD4+ T cells of sirolimus-treated mice. Simultaneously, sirolimus treatment led to a significant reduction in the number of CD4+ IL-17A+ T cells in the mesenteric lymph node cells as well as IL-17A production in mesenteric lymph node cells. Therefore, sirolimus may offer a promising new therapeutic strategy for the treatment of inflammatory bowel disease.</AbstractText>
<CopyrightInformation>© 2013 John Wiley & Sons Ltd.</CopyrightInformation>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yin</LastName>
<ForeName>Hui</ForeName>
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<AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Guangdong Pharmaceutical University, Guangzhou, China. huiyin0103@yahoo.com.cn</Affiliation>
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<ForeName>Xiangyong</ForeName>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Bobin</ForeName>
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<ForeName>Tao</ForeName>
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<Author ValidYN="Y"><LastName>Yuan</LastName>
<ForeName>Baohong</ForeName>
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