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Conference Paper: A role of interleukin-17A in modulating intracellular survival of Mycobacterium bovis BCG in murine macrophages

TitleA role of interleukin-17A in modulating intracellular survival of Mycobacterium bovis BCG in murine macrophages
Authors
Issue Date2013
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
The Annual Meeting of the American Association of Immunologists (AAI) on Immunology (Immunology 2013), Honolulu, Hawaii, 3-7 May 2013. In Journal of Immunology, 2013, v. 190 n. Meeting Abstract Supplement, p. abstract no. 130.8 How to Cite?
AbstractInterleukin-17A has been demonstrated to participate in the pathogenesis of mycobacterial infections. Whether interleukin-17A regulates innate defense mechanisms of macrophage against mycobacteria remain to be elucidated. In the present study, we investigated the effects of interleukin-17A on modulating the intracellular survival of Mycobacterium bovis BCG in RAW264.7 macrophages. Our data revealed that the clearance of intracellular BCG in macrophages was significantly enhanced by interleukin-17A pretreatment. Moreover, interleukin-17A-enhanced clearance of intracellular BCG could be abrogated by addition of inducible nitric oxide synthase inhibitor. We observed that interleukin-17A pretreatment was able to synergistically enhance both nitric oxide production and inducible nitric oxide synthase expression in BCG-infected macrophages in dose- and time-dependent manner. We also revealed that interleukin-17A was able to specifically enhance BCG-induced phosphorylation of JNK, but not ERK1/2 or p38 MAPK. By using specific JNK inhibitor SP600125, the production of nitric oxide in BCG-infected macrophages with interleukin-17A pretreatment was significantly suppressed. Taken together, we confirmed the involvement of JNK pathway in interleukin-17A-enhanced nitric oxide production in BCG-infected macrophages. In conclusion, our study revealed an anti-mycobacterial role of interleukin-17A through priming the macrophages to produce nitric oxide in response to mycobacteria infection.
Persistent Identifierhttp://hdl.handle.net/10722/206058
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549

 

DC FieldValueLanguage
dc.contributor.authorLing, WLen_US
dc.contributor.authorWang, Len_US
dc.contributor.authorPong, CHen_US
dc.contributor.authorLau, ASYen_US
dc.contributor.authorLi, CBen_US
dc.date.accessioned2014-10-20T11:47:26Z-
dc.date.available2014-10-20T11:47:26Z-
dc.date.issued2013en_US
dc.identifier.citationThe Annual Meeting of the American Association of Immunologists (AAI) on Immunology (Immunology 2013), Honolulu, Hawaii, 3-7 May 2013. In Journal of Immunology, 2013, v. 190 n. Meeting Abstract Supplement, p. abstract no. 130.8en_US
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10722/206058-
dc.description.abstractInterleukin-17A has been demonstrated to participate in the pathogenesis of mycobacterial infections. Whether interleukin-17A regulates innate defense mechanisms of macrophage against mycobacteria remain to be elucidated. In the present study, we investigated the effects of interleukin-17A on modulating the intracellular survival of Mycobacterium bovis BCG in RAW264.7 macrophages. Our data revealed that the clearance of intracellular BCG in macrophages was significantly enhanced by interleukin-17A pretreatment. Moreover, interleukin-17A-enhanced clearance of intracellular BCG could be abrogated by addition of inducible nitric oxide synthase inhibitor. We observed that interleukin-17A pretreatment was able to synergistically enhance both nitric oxide production and inducible nitric oxide synthase expression in BCG-infected macrophages in dose- and time-dependent manner. We also revealed that interleukin-17A was able to specifically enhance BCG-induced phosphorylation of JNK, but not ERK1/2 or p38 MAPK. By using specific JNK inhibitor SP600125, the production of nitric oxide in BCG-infected macrophages with interleukin-17A pretreatment was significantly suppressed. Taken together, we confirmed the involvement of JNK pathway in interleukin-17A-enhanced nitric oxide production in BCG-infected macrophages. In conclusion, our study revealed an anti-mycobacterial role of interleukin-17A through priming the macrophages to produce nitric oxide in response to mycobacteria infection.-
dc.languageengen_US
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org-
dc.relation.ispartofJournal of Immunologyen_US
dc.rightsThis is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (The AAI), publisher of The JI, holds the copyright to this manuscript. This manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence, it may differ from the final version published in The JI (online and in print). The AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.org-
dc.titleA role of interleukin-17A in modulating intracellular survival of Mycobacterium bovis BCG in murine macrophagesen_US
dc.typeConference_Paperen_US
dc.identifier.emailLing, WL: lingwl@graduate.hku.hken_US
dc.identifier.emailWang, L: vickyw@hku.hken_US
dc.identifier.emailPong, CH: jchpong@hku.hken_US
dc.identifier.emailLau, ASY: asylau@hku.hken_US
dc.identifier.emailLi, CB: jamesli@graduate.hku.hken_US
dc.identifier.authorityLau, ASY=rp00474en_US
dc.identifier.authorityLi, CB=rp00496en_US
dc.identifier.hkuros241338en_US
dc.identifier.volume190-
dc.identifier.issueMeeting Abstract Supplement-
dc.publisher.placeUnited States-

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