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Article: Activation of adenosine A3 receptor inhibits inflammatory cytokine production in colonic mucosa of patients with ulcerative colitis by down‐regulating the nuclear factor‐kappa B signaling

TitleActivation of adenosine A3 receptor inhibits inflammatory cytokine production in colonic mucosa of patients with ulcerative colitis by down‐regulating the nuclear factor‐kappa B signaling
Authors
Keywords2-Cl-IB-MECA
adenosine A3 receptor
NF-kappa B
ulcerative colitis
Issue Date2020
PublisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1751-2980
Citation
Journal of Digestive Diseases, 2020, v. 21 n. 1, p. 38-45 How to Cite?
AbstractObjectives: The activation of the adenosine A3 receptor (A3AR) can regulate inflammation, but the way that this regulates colonic mucosal inflammation in ulcerative colitis (UC) remains unclear. This study aimed at examining A3AR expression and investigating the effect of A3AR activation on ex vivo cytokine expression and nuclear factor-kappa B (NF-κB) signaling in colonic mucosa. Methods: Colonic mucosal biopsied tissue from 18 patients with UC and 11 healthy controls was tested for A3AR expression by immunofluorescence, quantitative real-time polymerase chain reaction and Western blot. Following treatment for 24 hours with or without 2-Cl-IB-MECA, an A3AR agonist, TNF-α and IL-1β secreted by the cultured colonic mucosal tissue were quantified by ELISA. The colonic mucosal epithelia were dissected and treated with, or without 2-Cl-IB-MECA for 24 hours. The NF-κB p65 protein and its distribution in the cultured colonic epithelia were examined by immunofluorescence and Western blot. Results: Compared with the controls, down-regulated A3AR expression and up-regulated TNF-α and IL-1β production and NF-κB p65 protein were observed in the UC colonic mucosa. The activation of A3AR by 2-Cl-IB-MECA significantly decreased TNF-α and IL-1β production and attenuated the NF-κB p65 activation in colonic tissues from patients with UC. Conclusions: A3AR activation inhibited inflammation by mitigating pro-inflammatory cytokine production and the NF-κB signal activation in colonic mucosa of patients with UC. A3AR activation may play a role in the pathogenesis of UC. © 2019 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd
Persistent Identifierhttp://hdl.handle.net/10722/280106
ISSN
2017 Impact Factor: 1.623
2015 SCImago Journal Rankings: 0.781
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRen, TH-
dc.contributor.authorLv, MM-
dc.contributor.authorAn, XM-
dc.contributor.authorLeung, WK-
dc.contributor.authorSeto, WK-
dc.date.accessioned2020-01-06T02:01:03Z-
dc.date.available2020-01-06T02:01:03Z-
dc.date.issued2020-
dc.identifier.citationJournal of Digestive Diseases, 2020, v. 21 n. 1, p. 38-45-
dc.identifier.issn1751-2972-
dc.identifier.urihttp://hdl.handle.net/10722/280106-
dc.description.abstractObjectives: The activation of the adenosine A3 receptor (A3AR) can regulate inflammation, but the way that this regulates colonic mucosal inflammation in ulcerative colitis (UC) remains unclear. This study aimed at examining A3AR expression and investigating the effect of A3AR activation on ex vivo cytokine expression and nuclear factor-kappa B (NF-κB) signaling in colonic mucosa. Methods: Colonic mucosal biopsied tissue from 18 patients with UC and 11 healthy controls was tested for A3AR expression by immunofluorescence, quantitative real-time polymerase chain reaction and Western blot. Following treatment for 24 hours with or without 2-Cl-IB-MECA, an A3AR agonist, TNF-α and IL-1β secreted by the cultured colonic mucosal tissue were quantified by ELISA. The colonic mucosal epithelia were dissected and treated with, or without 2-Cl-IB-MECA for 24 hours. The NF-κB p65 protein and its distribution in the cultured colonic epithelia were examined by immunofluorescence and Western blot. Results: Compared with the controls, down-regulated A3AR expression and up-regulated TNF-α and IL-1β production and NF-κB p65 protein were observed in the UC colonic mucosa. The activation of A3AR by 2-Cl-IB-MECA significantly decreased TNF-α and IL-1β production and attenuated the NF-κB p65 activation in colonic tissues from patients with UC. Conclusions: A3AR activation inhibited inflammation by mitigating pro-inflammatory cytokine production and the NF-κB signal activation in colonic mucosa of patients with UC. A3AR activation may play a role in the pathogenesis of UC. © 2019 Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine and John Wiley & Sons Australia, Ltd-
dc.languageeng-
dc.publisherWiley-Blackwell Publishing Asia. The Journal's web site is located at http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1751-2980-
dc.relation.ispartofJournal of Digestive Diseases-
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 Use of Self-Archived Versions. 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 Use of Self-Archived Versions.-
dc.subject2-Cl-IB-MECA-
dc.subjectadenosine A3 receptor-
dc.subjectNF-kappa B-
dc.subjectulcerative colitis-
dc.titleActivation of adenosine A3 receptor inhibits inflammatory cytokine production in colonic mucosa of patients with ulcerative colitis by down‐regulating the nuclear factor‐kappa B signaling-
dc.typeArticle-
dc.identifier.emailLeung, WK: waikleung@hku.hk-
dc.identifier.emailSeto, WK: wkseto@hku.hk-
dc.identifier.authorityLeung, WK=rp01479-
dc.identifier.authoritySeto, WK=rp01659-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/1751-2980.12831-
dc.identifier.pmid31714673-
dc.identifier.scopuseid_2-s2.0-85076734004-
dc.identifier.hkuros308879-
dc.identifier.volume21-
dc.identifier.issue1-
dc.identifier.spage38-
dc.identifier.epage45-
dc.identifier.isiWOS:000502948800001-
dc.publisher.placeAustralia-

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