Journals / The Anatolian Journal of Cardiology / 2020 / Cilt: 23 - Sayı: 3

The expression of interleukin-25 increases in human coronary artery disease and is associated with the severity of coronary stenosis

Pages
151–159
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

A receiver operator characteristic curve suggested that IL-25 presented a significantdiagnosis value in ACS.Conclusion: IL-25 is increased in the coronary arteries and serum of CAD patients and is associated with the severity of coronary stenosis andthe occurrence of ACS, suggesting that IL-25 may be one of the biomarkers of ACS.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Interleukin (IL) 25, also known as IL-17E, is an inflammatory cytokine and has been demonstrated to be closely related to cardiovascular diseases by regulating immunity and inflammation, including atherosclerosis.
📊
Key Findings & Data:This study was aimed to evaluate the expression of IL-25 inpatients with coronary artery disease (CAD).Methods: In this study, the expression of IL-25 in normal (n=6) and atherosclerotic (n=10) human coronary arteries was detected by immunofluorescent staining.
💡
Conclusion & Impact:A receiver operator characteristic curve suggested that IL-25 presented a significantdiagnosis value in ACS.Conclusion: IL-25 is increased in the coronary arteries and serum of CAD patients and is associated with the severity of coronary stenosis andthe occurrence of ACS, suggesting that IL-25 may be one of the biomarkers of ACS.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Objective: Interleukin (IL) 25, also known as IL-17E, is an inflammatory cytokine and has been demonstrated to be closely related to cardiovascular diseases by regulating immunity and inflammation, including atherosclerosis. This study was aimed to evaluate the expression of IL-25 inpatients with coronary artery disease (CAD).Methods: In this study, the expression of IL-25 in normal (n=6) and atherosclerotic (n=10) human coronary arteries was detected by immunofluorescent staining. In addition, the serum IL-25, IL-6, and tumor necrosis factor (TNF) α concentrations in stable angina pectoris (SAP, n=44),unstable angina pectoris (UAP, n=46), acute myocardial infarction (AMI, n=34), and non-CAD (control, n=36) were measured using enzyme-linkedimmunosorbent assay (ELISA) kits.Results: IL-25 was significantly increased in coronary arteries of CAD patients when compared with normal coronary arteries, with macrophages and T lymphocytes being the sources of IL-25, especially macrophages. Moreover, the serum concentrations of IL-25 were markedlyelevated in CAD patients and gradually increased in SAP, UAP, and AMI groups. In addition, IL-25 levels were positively correlated with the IL-6and TNF-α levels, and Gensini score in CAD patients. Logistic regression analysis showed that IL-25 was independently positively correlatedwith the occurrence of acute coronary syndrome (ACS). A receiver operator characteristic curve suggested that IL-25 presented a significantdiagnosis value in ACS.Conclusion: IL-25 is increased in the coronary arteries and serum of CAD patients and is associated with the severity of coronary stenosis andthe occurrence of ACS, suggesting that IL-25 may be one of the biomarkers of ACS.

🔖

Cite This Article

XU, Y., YE, J., WANG, M., LIU, J., WANG, Z., JIANG, H., YE, D., ZHANG, J., WAN, J. (2020). The expression of interleukin-25 increases in human coronary artery disease and is associated with the severity of coronary stenosis. The Anatolian Journal of Cardiology, Cilt: 23 - Sayı: 3, 151–159. https://ajindex.com/articles/365234

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (14)

  1. Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, et al.; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Executive summary: heart disease and stroke statistics--2012 update: a report from the American Heart Association. Circulation 2012; 125: 188-97
  2. Christodoulidis G, Vittorio TJ, Fudim M, Lerakis S, Kosmas CE. Inflammation in coronary artery disease. Cardiol Rev 2014; 22: 279-88
  3. Khan R, Spagnoli V, Tardif J, L'Allier PL. Novel anti-inflammatory therapies for the treatment of atherosclerosis. Atherosclerosis 2015; 240: 497-509
  4. Golia E, Limongelli G, Natale F, Fimiani F, Maddaloni V, Pariggiano I, et al. Inflammation and cardiovascular disease: from pathogenesis to therapeutic target. Curr Atheroscler Rep 2014; 16: 435
  5. Ridker PM, Everett BM, Thuren T, MacFadyen JG, Chang WH, Ballantyne C, et al.; CANTOS Trial Group. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N Engl J Med 2017; 377: 1119-31
  6. Ridker PM, MacFadyen JG, Thuren T, Everett BM, Libby P, Glynn RJ; CANTOS Trial Group. Effect of interleukin-1beta inhibition with canakinumab on incident lung cancer in patients with atherosclerosis: exploratory results from a randomised, double-blind, placebo-controlled trial. Lancet 2017; 390: 1833-42
  7. Kolls JK, Linden A. Interleukin-17 family members and inflammation. Immunity 2004; 21: 467-76
  8. Gu C, Wu L, Li X. IL-17 family: cytokines, receptors and signaling. Cytokine 2013; 64: 477-85
  9. Hashmi S, Zeng QT. Role of interleukin-17 and interleukin-17-induced cytokines interleukin-6 and interleukin-8 in unstable coronary artery disease. Coron Artery Dis 2006; 17: 699-706
  10. Liang J, Zheng Z, Wang M, Han L, Zheng Z, Peng J, et al. Myeloperoxidase (MPO) and interleukin-17 (IL-17) plasma levels are increased in patients with acute coronary syndromes. J Int Med Res 2009; 37: 862-6
  11. Avalos AM, Apablaza FA, Quiroz M, Toledo V, Pena JP, Michea L, et al. IL-17A levels increase in the infarcted region of the left ventricle in a rat model of myocardial infarction. Biol Res 2012; 45: 193-200
  12. Liao YH, Xia N, Zhou SF, Tang TT, Yan XX, Lv BJ, et al. Interleukin17A contributes to myocardial ischemia/reperfusion injury by regulating cardiomyocyte apoptosis and neutrophil infiltration. J Am Coll Cardiol 2012; 59: 420-9
  13. Harrington RA. Targeting Inflammation in Coronary Artery Disease. N Engl J Med 2017; 377: 1197-8
  14. Valizadeh A, Khosravi A, Zadeh LJ, Parizad