PMID- 26749303 OWN - NLM STAT- MEDLINE DCOM- 20170707 LR - 20210109 IS - 2326-5205 (Electronic) IS - 2326-5191 (Print) IS - 2326-5191 (Linking) VI - 68 IP - 6 DP - 2016 Jun TI - Brief Report: Proatherogenic Cytokine Microenvironment in the Aortic Adventitia of Patients With Rheumatoid Arthritis. PG - 1361-6 LID - 10.1002/art.39574 [doi] AB - OBJECTIVE: Patients with rheumatoid arthritis (RA) are at increased risk of developing cardiovascular disease (CVD) via mechanisms that have not yet been defined. Inflammatory pathways, in particular within the vascular adventitia, are implicated in the pathogenesis of primary CVD but could be amplified in RA at the local tissue level. The aim of this study was to examine the aortic adventitia of coronary artery disease (CAD) patients with or without RA to determine the cytokine profile contained therein. METHODS: Aortic adventitia and internal thoracic artery biopsy specimens obtained from 19 RA patients and 20 non-RA patients undergoing coronary artery bypass graft surgery were examined by immunohistochemistry. RESULTS: Interleukin-18 (IL-18), IL-33, and tumor necrosis factor (TNF) were expressed in aortic adventitia biopsy specimens from both groups, and expression of these cytokines was significantly higher in RA patients. In RA patients, IL-33 expression in endothelial cells correlated positively with the number of swollen joints, suggesting a link between the systemic disease state and the local vascular tissue microlesion. CONCLUSION: The presence of the proinflammatory cytokines IL-18, IL-33, and TNF may play a role in the inflammatory process within the adventitia that contributes to plaque formation and destabilization. In theory, the amplified expression of these cytokines may contribute to the known increased occurrence and severity of CAD in patients with RA. CI - (c) 2016 The Authors. Arthritis & Rheumatology published by Wiley Periodicals, Inc. on behalf of the American College of Rheumatology. FAU - Ahmed, Ammad AU - Ahmed A AD - University of Glasgow, Glasgow, UK. FAU - Hollan, Ivana AU - Hollan I AD - Hospital for Rheumatic Diseases, Lillehammer, Norway. FAU - Curran, Samuel A AU - Curran SA AD - University of Glasgow, Glasgow, UK. FAU - Kitson, Susan M AU - Kitson SM AD - University of Glasgow, Glasgow, UK. FAU - Riggio, Marcello P AU - Riggio MP AD - University of Glasgow, Glasgow, UK. FAU - Mikkelsen, Knut AU - Mikkelsen K AD - Hospital for Rheumatic Diseases, Lillehammer, Norway. FAU - Almdahl, Sven M AU - Almdahl SM AD - University Hospital of North Norway, Tromso, Norway. FAU - Aukrust, Pal AU - Aukrust P AD - Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway. FAU - McInnes, Iain B AU - McInnes IB AD - University of Glasgow, Glasgow, UK. FAU - Goodyear, Carl S AU - Goodyear CS AD - University of Glasgow, Glasgow, UK. LA - eng GR - 19701/ARC_/Arthritis Research UK/United Kingdom GR - 19701/VAC_/Versus Arthritis/United Kingdom PT - Journal Article PL - United States TA - Arthritis Rheumatol JT - Arthritis & rheumatology (Hoboken, N.J.) JID - 101623795 RN - 0 (IL33 protein, human) RN - 0 (Interleukin-18) RN - 0 (Interleukin-33) RN - 0 (Tumor Necrosis Factor-alpha) SB - IM MH - Adventitia/*chemistry MH - Aged MH - Aorta/*chemistry MH - Arthritis, Rheumatoid/*immunology MH - Atherosclerosis/immunology MH - Cellular Microenvironment MH - Female MH - Humans MH - Interleukin-18/*analysis MH - Interleukin-33/*analysis MH - Male MH - Tumor Necrosis Factor-alpha/*analysis PMC - PMC4920270 EDAT- 2016/01/11 06:00 MHDA- 2017/07/08 06:00 PMCR- 2016/06/24 CRDT- 2016/01/11 06:00 PHST- 2015/05/21 00:00 [received] PHST- 2015/12/29 00:00 [accepted] PHST- 2016/01/11 06:00 [entrez] PHST- 2016/01/11 06:00 [pubmed] PHST- 2017/07/08 06:00 [medline] PHST- 2016/06/24 00:00 [pmc-release] AID - ART39574 [pii] AID - 10.1002/art.39574 [doi] PST - ppublish SO - Arthritis Rheumatol. 2016 Jun;68(6):1361-6. doi: 10.1002/art.39574.