title: Recruitment of immune cells across atrial endocardium in human atrial fibrillation.
abstract: BACKGROUND
  Although clinical studies have suggested a link between inflammation markers and atrial fibrillation (AF), it is still unclear whether local immunologic responses actually exist in human atria during AF.
  
  
  RESULTS
  To address this point, human left appendages were obtained from 16 patients who underwent cardiac surgery (5 with sinus rhythm (SR) and 11 with AF) and subjected to immunohistochemical analysis. In all the AF specimens, adhesion and migration of CD45-reactive cells were consistently observed predominantly in the atrial endo- and subendomyocardium and more prominently than in SR. Most of them were immunologically active CD68-positive macrophages, whereas CD3-positive T cells infiltrated to a lesser extent. Scavenger-receptor A staining revealed maturation of macrophages not in the endocardium but in the midmyocardium, a gradient from endo- to midmyocardium. In the endocardium, along with adhesion molecules (intracellular adhesion molecule-1 and vascular cell adhesion molecule-1), a chemotactic protein-1, which facilitates the recruitment, was more abundantly expressed in AF than in SR. Cytokines including transforming growth factor-beta and interleukin-6 were frequently expressed by these macrophages.
  
  
  CONCLUSIONS
  These observations collectively imply active adhesion and recruitment of macrophages across the endocardium in human fibrillating atria, thereby supporting the concept of local immunologic inflammatory responses around the atrial endocardium of AF.
authors.affiliation: The Cardiovascular Institute, Tokyo, Japan. yamt-tky@umin.ac.jp
authors.forename: Takeshi
authors.initials: T
authors.lastname: Yamashita
authors.forename: Akiko
authors.initials: A
authors.lastname: Sekiguchi
authors.forename: Yu-ki
authors.initials: YK
authors.lastname: Iwasaki
authors.forename: Taro
authors.initials: T
authors.lastname: Date
authors.forename: Koichi
authors.initials: K
authors.lastname: Sagara
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Tanabe
authors.forename: Hisayoshi
authors.initials: H
authors.lastname: Suma
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Sawada
authors.forename: Tadanori
authors.initials: T
authors.lastname: Aizawa
mesh_terms: D056704:Adaptive Immunity; D000328:Adult; D000368:Aged; D015703:Antigens, CD / Q000032:analysis; D020517:Atrial Appendage / Q000276:immunology* / Q000473:pathology / Q000601:surgery; D001281:Atrial Fibrillation / Q000276:immunology* / Q000473:pathology / Q000601:surgery; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000032:analysis; D002465:Cell Movement; D016207:Cytokines / Q000032:analysis; D004699:Endocardium / Q000276:immunology* / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007113:Immunity, Innate; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000032:analysis*; D008264:Macrophages / Q000276:immunology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D051117:Scavenger Receptors, Class A / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology
chemical_list: D015703:Antigens, CD; D015815:Cell Adhesion Molecules; D016207:Cytokines; D018836:Inflammation Mediators; D051117:Scavenger Receptors, Class A