title: Increased M1 Macrophages Infiltration Is Associated with Thrombogenesis in Rheumatic Mitral Stenosis Patients with Atrial Fibrillation.
abstract: Atrial fibrillation (AF) is the most common arrhythmia. In patients with AF, the role of macrophage subsets in thrombogenesis is unclear. In the present study, we analyzed the role of M1 and M2 macrophages and related cytokines in thrombogenesis of AF. Immunohistochemistry, Western blot, and TUNEL assay were used to detect M1/M2 macrophage infiltration, the expression pattern of IL-1β and inflammasome components, and apoptosis of cardiomyocytes in 71 specimens obtained from the left atrial appendage of patients with rheumatic mitral stenosis (MS) with or without thrombosis. We demonstrated that proinflammatory M1 macrophages were predominant in the atrium of MS patients with AF and thrombus. NLRP3 inflammasomes and IL-1β, which are primarily functional in macrophages, were activated in those patients. We also showed that increased cell death was associated with thrombogenesis in MS patients. These data indicate that infiltration of M1 macrophages and over-activation of NLRP3 inflammasomes may play a role in progressive atrial inflammation and thrombogenesis in rheumatic mitral stenosis patients with AF.
authors.affiliation: Department of Cardiology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.|Department of Cardiology, the First Affiliated Hospitol of Guangxi University of Chinese Medicine, Nanning, China.
authors.forename: Guixin
authors.initials: G
authors.lastname: He
authors.affiliation: Department of Cardiology, the First Affiliated Hospitol of Guangxi University of Chinese Medicine, Nanning, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Tan
authors.affiliation: Department of Cardiology, Huaian First People's Hospital, Huaian, China.
authors.forename: Bingjian
authors.initials: B
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.
authors.forename: Jianzhou
authors.initials: J
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.
authors.forename: Guannan
authors.initials: G
authors.lastname: Li
authors.affiliation: Department of Cardiology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.
authors.forename: Suhui
authors.initials: S
authors.lastname: Zhu
authors.affiliation: Department of Cardiology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.
authors.forename: Jun
authors.initials: J
authors.lastname: Xie
authors.affiliation: Department of Cardiology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, China.
authors.forename: Biao
authors.initials: B
authors.lastname: Xu
mesh_terms: D000328:Adult; D001281:Atrial Fibrillation / Q000150:complications* / Q000276:immunology / Q000473:pathology; D002352:Carrier Proteins / Q000032:analysis / Q000276:immunology; D005260:Female; D006801:Humans; D058847:Inflammasomes / Q000032:analysis / Q000276:immunology; D053583:Interleukin-1beta / Q000032:analysis / Q000276:immunology; D008264:Macrophages / Q000276:immunology / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D008946:Mitral Valve Stenosis / Q000150:complications* / Q000276:immunology / Q000473:pathology; D032383:Myocytes, Cardiac / Q000276:immunology / Q000473:pathology; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D012214:Rheumatic Heart Disease / Q000150:complications* / Q000276:immunology / Q000473:pathology; D013927:Thrombosis / Q000150:complications* / Q000276:immunology / Q000473:pathology
chemical_list: D002352:Carrier Proteins; D058847:Inflammasomes; D053583:Interleukin-1beta; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C453881:NLRP3 protein, human