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Article: Leptin exacerbates collagen-induced arthritis via enhancement of Th17 cell response

TitleLeptin exacerbates collagen-induced arthritis via enhancement of Th17 cell response
Authors
Issue Date2012
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/
Citation
Arthritis & Rheumatism, 2012, v. 64 n. 11, p. 3564-3573 How to Cite?
AbstractOBJECTIVE: To determine the role of leptin in modulating Th17 cell response and joint inflammation in mice with collagen-induced arthritis (CIA). METHODS: Leptin receptor expression on T cells was examined by polymerase chain reaction (PCR) analysis, immunofluorescence microscopy, and flow cytometry. Effects of leptin on Th17 cell differentiation and proliferation were evaluated by quantitative PCR, carboxyfluorescein diacetate succinimidyl ester proliferation assay, and flow cytometry. Dynamic changes in leptin concentrations in the joint tissue and synovial fluid of mice with CIA were determined by immunohistochemistry analysis and enzyme-linked immunosorbent assay (ELISA). Arthritis symptoms and joint pathology in mice with CIA were assessed after injection of leptin into the knee joint. Th1 and Th17 cell populations in the spleen, draining lymph nodes, and joint tissue were analyzed by flow cytometry and enzyme-linked immunospot assay. Interleukin-17 messenger RNA and protein levels in the joint tissue were measured by PCR analysis and ELISA. RESULTS: In culture, leptin treatment significantly increased Th17 cell generation from naive CD4+ T cells. During CIA development, markedly elevated levels of leptin were detected in the joint tissue and synovial fluid. Moreover, injection of leptin into the knee joint of collagen-immunized mice resulted in an early onset of arthritis and substantially increased the severity of clinical symptoms, accompanied by more pronounced synovial hyperplasia and joint damage. Further examination by immunofluorescence microscopy confirmed the presence of significantly increased numbers of Th17 cells in the joint tissue and draining lymph nodes of leptin-treated mice with CIA. CONCLUSION: The results of this study identify a previously undescribed function of leptin in enhancing Th17 cell response and exacerbating joint inflammation in mice with CIA.
Persistent Identifierhttp://hdl.handle.net/10722/186441
ISSN
2015 Impact Factor: 8.955
2015 SCImago Journal Rankings: 3.206
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorDeng, J-
dc.contributor.authorLiu, Y-
dc.contributor.authorYang, M-
dc.contributor.authorWang, S-
dc.contributor.authorZhang, M-
dc.contributor.authorWang, X-
dc.contributor.authorKo, KH-
dc.contributor.authorHua, Z-
dc.contributor.authorSun, L-
dc.contributor.authorCao, X-
dc.contributor.authorLu, L-
dc.date.accessioned2013-08-20T12:09:01Z-
dc.date.available2013-08-20T12:09:01Z-
dc.date.issued2012-
dc.identifier.citationArthritis & Rheumatism, 2012, v. 64 n. 11, p. 3564-3573-
dc.identifier.issn0004-3591-
dc.identifier.urihttp://hdl.handle.net/10722/186441-
dc.description.abstractOBJECTIVE: To determine the role of leptin in modulating Th17 cell response and joint inflammation in mice with collagen-induced arthritis (CIA). METHODS: Leptin receptor expression on T cells was examined by polymerase chain reaction (PCR) analysis, immunofluorescence microscopy, and flow cytometry. Effects of leptin on Th17 cell differentiation and proliferation were evaluated by quantitative PCR, carboxyfluorescein diacetate succinimidyl ester proliferation assay, and flow cytometry. Dynamic changes in leptin concentrations in the joint tissue and synovial fluid of mice with CIA were determined by immunohistochemistry analysis and enzyme-linked immunosorbent assay (ELISA). Arthritis symptoms and joint pathology in mice with CIA were assessed after injection of leptin into the knee joint. Th1 and Th17 cell populations in the spleen, draining lymph nodes, and joint tissue were analyzed by flow cytometry and enzyme-linked immunospot assay. Interleukin-17 messenger RNA and protein levels in the joint tissue were measured by PCR analysis and ELISA. RESULTS: In culture, leptin treatment significantly increased Th17 cell generation from naive CD4+ T cells. During CIA development, markedly elevated levels of leptin were detected in the joint tissue and synovial fluid. Moreover, injection of leptin into the knee joint of collagen-immunized mice resulted in an early onset of arthritis and substantially increased the severity of clinical symptoms, accompanied by more pronounced synovial hyperplasia and joint damage. Further examination by immunofluorescence microscopy confirmed the presence of significantly increased numbers of Th17 cells in the joint tissue and draining lymph nodes of leptin-treated mice with CIA. CONCLUSION: The results of this study identify a previously undescribed function of leptin in enhancing Th17 cell response and exacerbating joint inflammation in mice with CIA.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/-
dc.relation.ispartofArthritis & Rheumatism-
dc.rightsArthritis & Rheumatism. Copyright © John Wiley & Sons, Inc.-
dc.rightsPreprint: This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving. Postprint: This is the peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving. Special Statement for Preprint only Before publication: 'This is a preprint of an article accepted for publication in [The Journal of Pathology] Copyright © ([year]) ([Pathological Society of Great Britain and Ireland])'. After publication: the preprint notice should be amended to follows: 'This is a preprint of an article published in [include the complete citation information for the final version of the Contribution as published in the print edition of the Journal]' For Cochrane Library/ Cochrane Database of Systematic Reviews, add statement & acknowledgement : ‘This review is published as a Cochrane Review in the Cochrane Database of Systematic Reviews 20XX, Issue X. Cochrane Reviews are regularly updated as new evidence emerges and in response to comments and criticisms, and the Cochrane Database of Systematic Reviews should be consulted for the most recent version of the Review.’ Please include reference to the Review and hyperlink to the original version using the following format e.g. Authors. Title of Review. Cochrane Database of Systematic Reviews 20XX, Issue #. Art. No.: CD00XXXX. DOI: 10.1002/14651858.CD00XXXX (insert persistent link to the article by using the URL: http://dx.doi.org/10.1002/14651858.CD00XXXX) (This statement should refer to the most recent issue of the Cochrane Database of Systematic Reviews in which the Review published.)-
dc.subject.meshArthritis, Experimental - immunology - metabolism - pathology-
dc.subject.meshInterleukin-17 - genetics - immunology-
dc.subject.meshLeptin - genetics - immunology - pharmacology-
dc.subject.meshLymph Nodes - immunology - pathology-
dc.subject.meshTh17 Cells - cytology - drug effects - immunology-
dc.titleLeptin exacerbates collagen-induced arthritis via enhancement of Th17 cell response-
dc.typeArticle-
dc.identifier.emailKo, KH: khko@hku.hk-
dc.identifier.emailLu, L: liweilu@hkucc.hku.hk-
dc.identifier.authorityLu, L=rp00477-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/art.34637-
dc.identifier.pmid22833425-
dc.identifier.hkuros218877-
dc.identifier.volume64-
dc.identifier.issue11-
dc.identifier.spage3564-
dc.identifier.epage3573-
dc.identifier.isiWOS:000310544500010-
dc.publisher.placeUnited States-

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