title: Enhancing anti-inflammatory cytokine IL-10 may be beneficial for acute coronary syndrome.
abstract: Inflammation is one of the basic biological responses against vascular injury. It has been demonstrated, however, that inflammation is an important pathogenic feature in atherosclerotic lesions. Previous data showed that pro-inflammatory cytokines played an important role in acute coronary events. A complex intravascular inflammatory response is also an integral component of atherosclerotic plaque dynamic instability, and the imbalance between anti-inflammatory mechanisms and pro-inflammatory factors, in favor of the pro-inflammatory factors, will result in rupture of atherosclerotic plaque. Interluekine-10 (IL-10), which is produced by various inflammatory cells, especially macrophages, has multifaceted anti-inflammatory properties, including inhibition of the prototypic pro-inflammatory transcription factor nuclear factor-kappaB, leading to suppressed cytokine production, inhibition of matrix degrading metalloproteinase production, reduction of tissue factor expression, inhibition of apoptosis of macrophages and monocytes after infection, and promotion of the phenotypic switch of lymphocytes into the Th2 phenotype. All these inflammatory mechanisms have been shown to play a pivotal role for atheroslerotic lesion development and progression, indicating a potential regulatory role of IL-10. More recent data showed that decreased plasma concentration of anti-inflammatory cytokine IL-10 was associated with acute coronary syndrome. Therefore, we hypotheses that enhancing anti-inflammatory cytokine IL-10 may be a promising approach for the therapy of acute coronary diseases.
authors.affiliation: Department of Cardiology, Fu Wai Hospital and Cardiovascular Institute, Chinese Academy of Medical Science and Peking Union Medical College, Beilishi Road 167, Beijing 100037, People's Republic of China. lijnjn@yahoo.com.cn
authors.forename: Jian-Jun
authors.initials: JJ
authors.lastname: Li
authors.forename: Yuan-Lin
authors.initials: YL
authors.lastname: Guo
authors.forename: Yue-Jin
authors.initials: YJ
authors.lastname: Yang
mesh_terms: D000208:Acute Disease; D000789:Angina, Unstable / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D001161:Arteriosclerosis / Q000473:pathology; D003327:Coronary Disease / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D016207:Cytokines / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D016753:Interleukin-10 / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D061965:Matrix Metalloproteinase Inhibitors; D008954:Models, Biological; D016328:NF-kappa B / Q000037:antagonists & inhibitors
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D061965:Matrix Metalloproteinase Inhibitors; D016328:NF-kappa B; D016753:Interleukin-10