Superoxide production and enhanced NOX2 induction through JAK/STAT signalling mediate IL-6-induced inflammatory responses of colon epithelial cells
DC Field | Value | Language |
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dc.contributor.author | Grung, P. | - |
dc.contributor.author | Banskota, S. | - |
dc.contributor.author | Jeong, B-S. | - |
dc.contributor.author | Nam, T-G. | - |
dc.contributor.author | Kim, J-A. | - |
dc.date.accessioned | 2021-06-22T12:21:47Z | - |
dc.date.available | 2021-06-22T12:21:47Z | - |
dc.date.created | 2021-01-21 | - |
dc.date.issued | 2018-02 | - |
dc.identifier.issn | 1873-9946 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/6808 | - |
dc.description.abstract | Background IL-6 plays an important role in the pathogenesis of inflammatory bowel disease (IBD), which is supported by close correlation between IL-6 production and severity of the disease in IBD patients. IL-6 enhances expression of adhesion molecules that are required for the recruitment process of neutrophils and monocytes to lesion sites. The regulation of those molecule expressions by NF-κB, a redox-sensitive transcription factor, implies that IL-6-induced adhesion molecule expression may also be associated with reactive oxygen species (ROS) producing activity of IL-6. Present study focused on whether NADPH oxidase is involved in IL-6-induced ROS production and changes in the protein expressions. Methods The IL-6-induced adhesion of monocytes (U937 cell line) to colon epithelial cells (HT-29 cell line) was examined by co-culture of HT-29 cells with U937 cells that were already labelled with BCECF-AM (10 μg/ml). After 3 h treatment with IL-6, BCECF fluorescence from adhered cells was measured. To identify signalling pathway, siRNA transfection, RT-PCR and Western blot analyses were performed. ROS was measured by lucigenin chemiluminescence assay. Results IL-6 significantly increased U937 monocytic cell adhesion to HT-29 colonic epithelial cells, which was accompanied by upregulation of adhesion molecules (ICAM-1 and VCAM-1) and repression of junction proteins (E-cadherin and claudin). Concurrently, IL-6 significantly increased superoxide production in a time-dependent manner, which matched significant induction of NOX2 and its regulatory subunits. The IL-6-induced ROS production and protein expression changes were attenuated by pretreatment with NADPH oxidase inhibitors (VAS-2840, and DPI) and STAT3 inhibitor (stattic), but not by inhibitors against other enzymes, such as cytosolic COX-2 (celecoxib), mitochondria (antimycin A), xanthine oxidase (allopurinol), and iNOS (NAME). Similarly, tofacitinib, a JAK inhibitor, and sttattic blocked IL-6-induced superoxide production and NOX2 induction. Conclusions Taken together, our results suggest that IL-6-activated JAK/STAT signalling is linked to superoxide production and NOX2 induction, resulting in IL-6-induced inflammatory responses of colon epithelial cells. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | OXFORD UNIV PRESS | - |
dc.title | Superoxide production and enhanced NOX2 induction through JAK/STAT signalling mediate IL-6-induced inflammatory responses of colon epithelial cells | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Nam, T-G. | - |
dc.identifier.doi | 10.1093/ecco-jcc/jjx180.174 | - |
dc.identifier.wosid | 000427318900174 | - |
dc.identifier.bibliographicCitation | JOURNAL OF CROHNS & COLITIS, v.12, pp.S115 - S116 | - |
dc.relation.isPartOf | JOURNAL OF CROHNS & COLITIS | - |
dc.citation.title | JOURNAL OF CROHNS & COLITIS | - |
dc.citation.volume | 12 | - |
dc.citation.startPage | S115 | - |
dc.citation.endPage | S116 | - |
dc.type.rims | ART | - |
dc.type.docType | Meeting Abstract | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Gastroenterology & Hepatology | - |
dc.relation.journalWebOfScienceCategory | Gastroenterology & Hepatology | - |
dc.identifier.url | https://academic.oup.com/ecco-jcc/article/12/supplement_1/S115/4807617 | - |
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