Background Coronary artery calcification （CAC） is a predictor of cardiovascular events and plaque burden and is closely associatedwith chronic inflammation. Intedeukin （IL）-37 is a newly discovered member of the I...Background Coronary artery calcification （CAC） is a predictor of cardiovascular events and plaque burden and is closely associatedwith chronic inflammation. Intedeukin （IL）-37 is a newly discovered member of the IL-1 family and is considered an anti-inflammatorycytokine. Our recent study on mice indicated that IL-37 could attenuate atherosclerosis and vascular calcification, which suggests that IL-37could be associated with the development of atherosclerosis and related diseases. The aim of this study was to investigate if IL-37 plays arole in the progression of CAC in patients. Methods Two hundred participants with suspected cardiovascular disease were recruited. Thelevels of plasma IL-37, osteoprotegerin （OPG）, hypersensitive C-reactive protein （hsCRP） together with other biochemical parameters weremeasured, and a coronary calcium assessment was carried out by multi-detector row CT. A score of 〈 10 AU （Agatston units） denotes anabsence of CAC, a score of 11-100 AU denotes mild CAC, 101-400 denotes moderate CAC, and 〉 400 AU denotes severe CAC. ResultsOur initial data showed that there were no apparent differences in plasma IL-37 levels among patients with or without mild or moderate CAC.However, IL-37 levels were significantly increased in patients with severe CAC （P 〈 0.001）. Similar results were observed for plasma OPGand hsCRP levels. When IL-37 levels in patients with severe calcification were compared with that in all of the other non-severe CAC groups,it became apparent that there was a significant positive correlation between IL-37 level and severe CAC （r = 0.360, P 〈 0.001; OR = 1.033）using Spearrnan＇s correlation and binary logistic regression analysis. Conclusions This study demonstrates that the anti-inflammatory cy-tokine IL-37 is associated with high coronary calcium levels, suggesting that IL-37 expression may be caused by the activation ofinf/amma-tion and that IL-37 might become a predictor of severe CAC in the future, which requires further investigation.展开更多
AIM:To investigate Toll-like receptor(TLR)signaling regulators in microscopic and ulcerative colitis patients.METHODS:Total RNA and microRNA were isolated from fresh frozen colonic biopsies of non-inflamed controls an...AIM:To investigate Toll-like receptor(TLR)signaling regulators in microscopic and ulcerative colitis patients.METHODS:Total RNA and microRNA were isolated from fresh frozen colonic biopsies of non-inflamed controls and patients with active or in-remission collagenous colitis(CC),lymphocytic colitis(LC),or ulcerative colitis(UC).We compared expressions of interleukin-1receptor-associated kinase(IRAK)-2,IRAK-M,interleukin(IL)-37,microRNA(miR)-146a,miR-155,and miR-21 using quantitative real time reverse transcription polymerase chain reaction.RESULTS:IRAK-M expression was increased in LC patients with active disease in histopathological remission(LC-HR;P=0.02)and UC patients(P=0.01),but no differences in IRAK-2 expression were detected compared to controls.miR-146a,-155 and-21 expressions were increased in LC-HR(P=0.04,0.07,and 0.004)and UC(P=0.02,0.04 and 0.03)patients.miR-146a and miR-21 expressions were significantly enhanced in UC patients compared to UC remission(UC-R;P=0.01and 0.04).Likewise,active CC patients showed significantly increased expression of miR-155(P=0.003)and miR-21(P=0.006).IL-37 expression was decreased in both CC(P=0.03)and LC(P=0.04)patients with a similar trend in UC patients but not statistically significant,whilst it was increased in UC-R patients compared to controls(P=0.02)and active UC(P=0.001).CONCLUSION:The identification of differentially expressed miRNAs,IL-37,and IRAK-M suggests different pathophysiologic mechanisms in various disease stages in LC,CC,and UC.展开更多
文摘Background Coronary artery calcification （CAC） is a predictor of cardiovascular events and plaque burden and is closely associatedwith chronic inflammation. Intedeukin （IL）-37 is a newly discovered member of the IL-1 family and is considered an anti-inflammatorycytokine. Our recent study on mice indicated that IL-37 could attenuate atherosclerosis and vascular calcification, which suggests that IL-37could be associated with the development of atherosclerosis and related diseases. The aim of this study was to investigate if IL-37 plays arole in the progression of CAC in patients. Methods Two hundred participants with suspected cardiovascular disease were recruited. Thelevels of plasma IL-37, osteoprotegerin （OPG）, hypersensitive C-reactive protein （hsCRP） together with other biochemical parameters weremeasured, and a coronary calcium assessment was carried out by multi-detector row CT. A score of 〈 10 AU （Agatston units） denotes anabsence of CAC, a score of 11-100 AU denotes mild CAC, 101-400 denotes moderate CAC, and 〉 400 AU denotes severe CAC. ResultsOur initial data showed that there were no apparent differences in plasma IL-37 levels among patients with or without mild or moderate CAC.However, IL-37 levels were significantly increased in patients with severe CAC （P 〈 0.001）. Similar results were observed for plasma OPGand hsCRP levels. When IL-37 levels in patients with severe calcification were compared with that in all of the other non-severe CAC groups,it became apparent that there was a significant positive correlation between IL-37 level and severe CAC （r = 0.360, P 〈 0.001; OR = 1.033）using Spearrnan＇s correlation and binary logistic regression analysis. Conclusions This study demonstrates that the anti-inflammatory cy-tokine IL-37 is associated with high coronary calcium levels, suggesting that IL-37 expression may be caused by the activation ofinf/amma-tion and that IL-37 might become a predictor of severe CAC in the future, which requires further investigation.
基金Research Committee of Orebro County CouncilSezin Gunaltay's salary is covered by a grant from Orebro University
文摘AIM:To investigate Toll-like receptor(TLR)signaling regulators in microscopic and ulcerative colitis patients.METHODS:Total RNA and microRNA were isolated from fresh frozen colonic biopsies of non-inflamed controls and patients with active or in-remission collagenous colitis(CC),lymphocytic colitis(LC),or ulcerative colitis(UC).We compared expressions of interleukin-1receptor-associated kinase(IRAK)-2,IRAK-M,interleukin(IL)-37,microRNA(miR)-146a,miR-155,and miR-21 using quantitative real time reverse transcription polymerase chain reaction.RESULTS:IRAK-M expression was increased in LC patients with active disease in histopathological remission(LC-HR;P=0.02)and UC patients(P=0.01),but no differences in IRAK-2 expression were detected compared to controls.miR-146a,-155 and-21 expressions were increased in LC-HR(P=0.04,0.07,and 0.004)and UC(P=0.02,0.04 and 0.03)patients.miR-146a and miR-21 expressions were significantly enhanced in UC patients compared to UC remission(UC-R;P=0.01and 0.04).Likewise,active CC patients showed significantly increased expression of miR-155(P=0.003)and miR-21(P=0.006).IL-37 expression was decreased in both CC(P=0.03)and LC(P=0.04)patients with a similar trend in UC patients but not statistically significant,whilst it was increased in UC-R patients compared to controls(P=0.02)and active UC(P=0.001).CONCLUSION:The identification of differentially expressed miRNAs,IL-37,and IRAK-M suggests different pathophysiologic mechanisms in various disease stages in LC,CC,and UC.
