title: Decreased myocardial dendritic cells is associated with impaired reparative fibrosis and development of cardiac rupture after myocardial infarction in humans.
abstract: BACKGROUND
  Dendritic cells (DC) play pivotal roles in regulating the immune system and inflammatory response. We previously reported DC infiltration in the infarcted heart and its immunoprotective roles in the post-infarction healing process after experimental myocardial infarction (MI). However, its clinical significance has not been determined.
  
  
  RESULTS
  The degree of DC infiltration and its correlation with the post-infarction healing process in the human infarcted heart were investigated in 24 autopsy subjects after ST-elevation MI. Patients were divided into two groups according to the presence (n=13) or absence (n=11) of cardiac rupture. The numbers of infiltrated DC and macrophages and the extent of fibrosis in the infarcted area were examined. In the rupture group, CD68(+) macrophage infiltration was increased and CD209(+) DC, and CD11c(+) DC infiltration and the extent of reparative fibrosis were decreased compared with the non-rupture group, under matched baseline characteristics including the time from onset to death and use of revascularization. Furthermore, there was a significant positive correlation between the number of infiltrating CD209(+) DC, and CD11c(+) DC and the extent of reparative fibrosis.
  
  
  CONCLUSIONS
  Decreased number of DC in human-infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI. These findings suggest a protective role of DC in post-MI inflammation and the subsequent healing process.
authors.affiliation: Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (T.N., S.H., Y.S., Y.A., K.K., M.I., S.Y., H.O., T.A.).
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Nagai
authors.affiliation: Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (T.N., S.H., Y.S., Y.A., K.K., M.I., S.Y., H.O., T.A.).
authors.forename: Satoshi
authors.initials: S
authors.lastname: Honda
authors.affiliation: Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (T.N., S.H., Y.S., Y.A., K.K., M.I., S.Y., H.O., T.A.).
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Sugano
authors.affiliation: Department of Clinical Pathology, National Cerebral and Cardiovascular Center, Osaka, Japan (T.M., K.O.O., Y.I., H.I.U.).
authors.forename: Taka-aki
authors.initials: TA
authors.lastname: Matsuyama
authors.affiliation: Department of Clinical Pathology, National Cerebral and Cardiovascular Center, Osaka, Japan (T.M., K.O.O., Y.I., H.I.U.).
authors.forename: Keiko
authors.initials: K
authors.lastname: Ohta-Ogo
authors.affiliation: Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (T.N., S.H., Y.S., Y.A., K.K., M.I., S.Y., H.O., T.A.).
authors.forename: Yasuhide
authors.initials: Y
authors.lastname: Asaumi
authors.affiliation: Department of Clinical Pathology, National Cerebral and Cardiovascular Center, Osaka, Japan (T.M., K.O.O., Y.I., H.I.U.).
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Ikeda
authors.affiliation: Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (T.N., S.H., Y.S., Y.A., K.K., M.I., S.Y., H.O., T.A.).
authors.forename: Kengo
authors.initials: K
authors.lastname: Kusano
authors.affiliation: Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (T.N., S.H., Y.S., Y.A., K.K., M.I., S.Y., H.O., T.A.).
authors.forename: Masaharu
authors.initials: M
authors.lastname: Ishihara
authors.affiliation: Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (T.N., S.H., Y.S., Y.A., K.K., M.I., S.Y., H.O., T.A.).
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yasuda
authors.affiliation: Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (T.N., S.H., Y.S., Y.A., K.K., M.I., S.Y., H.O., T.A.) Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan (H.O.).
authors.forename: Hisao
authors.initials: H
authors.lastname: Ogawa
authors.affiliation: Department of Clinical Pathology, National Cerebral and Cardiovascular Center, Osaka, Japan (T.M., K.O.O., Y.I., H.I.U.).
authors.forename: Hatsue
authors.initials: H
authors.lastname: Ishibashi-Ueda
authors.affiliation: Department of Cardiovascular Medicine, National Cerebral and Cardiovascular Center, Osaka, Japan (T.N., S.H., Y.S., Y.A., K.K., M.I., S.Y., H.O., T.A.).
authors.forename: Toshihisa
authors.initials: T
authors.lastname: Anzai
mesh_terms: D000368:Aged; D015703:Antigens, CD / Q000502:physiology; D015214:Antigens, Differentiation, Myelomonocytic / Q000502:physiology; D016022:Case-Control Studies; D015815:Cell Adhesion Molecules / Q000502:physiology; D003713:Dendritic Cells / Q000473:pathology* / Q000502:physiology; D005260:Female; D005355:Fibrosis; D006321:Heart / Q000503:physiopathology; D006342:Heart Rupture, Post-Infarction / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D037181:Lectins, C-Type / Q000502:physiology; D008264:Macrophages / Q000473:pathology / Q000502:physiology; D008297:Male; D009203:Myocardial Infarction / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000166:cytology / Q000473:pathology*; D011956:Receptors, Cell Surface / Q000502:physiology; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D015815:Cell Adhesion Molecules; D037181:Lectins, C-Type; D011956:Receptors, Cell Surface; D000099215:DC-Specific ICAM-3 Grabbing Nonintegrin; C067980:CD68 antigen, human; D000097382:CD68 Molecule
keywords: cardiac rupture; dendritic cell; inflammation; myocardial infarction; reparative fibrosis