title: Infiltration of macrophages through the atrial endocardium of inflammation-induced rats: contribution of fractalkine.
abstract: BACKGROUND
  Inflammatory processes in the atria during systemic inflammation remain unclear, so this study tested the hypothesis that macrophages infiltrate the atrial myocardium mainly through the atrial endocardium with the contribution of fractalkine.
  
  
  RESULTS
  Sprague-Dawley rats were injected with lipopolysaccharide (LPS) to simulate inflammation in the atria. Inflammation was immunohistologically assessed by the presence of macrophages. Macrophage infiltration was diffuse throughout the atrial myocardium after LPS injection. At an earlier phase after LPS injection, the number of macrophages dramatically increased, mainly in the atrial endocardium, and the expression of fractalkine protein was markedly increased by treatment with LPS in the atrial endocardium. The LPS-induced increase in atrial macrophage infiltration was significantly suppressed by neutralizing the fractalkine protein (P<0.01).
  
  
  CONCLUSIONS
  In an experimental model of atrial inflammation, macrophages infiltrated the myocardium mainly through the atrial endocardium with the contribution of fractalkine. Inhibition of macrophage infiltration by suppressing chemokine expression could be a novel therapeutic approach to controling acute inflammation in the atria.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Jikei University School of Medicine, Tokyo, Japan. datet@jikei.ac.jp
authors.forename: Taro
authors.initials: T
authors.lastname: Date
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: Tadanori
authors.initials: T
authors.lastname: Aizawa
authors.forename: Teiichi
authors.initials: T
authors.lastname: Yamane
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Aramaki
authors.forename: Kimiaki
authors.initials: K
authors.lastname: Komukai
authors.forename: Ikuo
authors.initials: I
authors.lastname: Taniguchi
authors.forename: Michihiro
authors.initials: M
authors.lastname: Yoshimura
mesh_terms: D000818:Animals; D000906:Antibodies / Q000008:administration & dosage; D054428:Chemokine CX3CL1 / Q000378:metabolism*; D002633:Chemotaxis; D004195:Disease Models, Animal; D004699:Endocardium / Q000276:immunology*; D006325:Heart Atria / Q000276:immunology; D007249:Inflammation / Q000139:chemically induced / Q000276:immunology*; D007274:Injections, Intraperitoneal; D008070:Lipopolysaccharides; D008264:Macrophages / Q000276:immunology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000906:Antibodies; D054428:Chemokine CX3CL1; C515540:Cx3cl1 protein, rat; D008070:Lipopolysaccharides