title: The role of infection in the development of non-valvular atrial fibrillation: up-regulation of Toll-like receptor 2 expression levels on monocytes.
abstract: Many studies have suggested that inflammation may participate in the pathogenesis of non-valvular atrial fibrillation (AF). However, it has been unknown by exposure to what the inflammation is caused. Recently, we reported that Toll-like receptor 2 (TLR2) level on monocytes was significantly up-regulated in viral and bacterial infections, but not in non-infectious inflammatory states. Our purpose was to test the hypothesis that expression of TLR2 levels may be up-regulated in patients with non-valvular AF. A total of 48 consecutive patients with non-valvular AF who were hospitalized for catheter ablation were enrolled in this study. TLR2 levels were assayed by using flow-cytometric analysis and compared with volunteers in sinus rhythm (control group, n = 24). Additionally, C-reactive protein (CRP) and interleukin-6 (IL-6) levels were assayed, and the left atrial volume indexes (LAVI) in the non-valvular AF group were measured. The results demonstrated that TLR2 levels in the non-valvular AF group were significantly higher than in the control group (median, 4682 vs. 3866 sites/cell; P < 0.01). Moreover, non-valvular AF patients had significantly higher IL-6 levels than controls. However, there was no significant difference in CRP levels between the two groups. It was observed in 44 AF patients, in whom pulmonary vein isolation was confirmed to be successful, that the LAVI significantly diminished 1 month after ablation (median, 33.6 vs. 29.5 ml/m²; P < 0.001), but not the TLR2 and IL-6 levels. Our results implied that an infectious inflammation may participate in the pathogenesis of non-valvular AF.
authors.affiliation: Department of Cardiovascular, Respiratory & Metabolic Medicine, Graduate School of Medicine, Kagoshima University, Kagoshima, Japan.
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ichiki
authors.forename: Koji
authors.initials: K
authors.lastname: Orihara
authors.forename: Shuichi
authors.initials: S
authors.lastname: Hamasaki
authors.forename: Sanemasa
authors.initials: S
authors.lastname: Ishida
authors.forename: Naoya
authors.initials: N
authors.lastname: Oketani
authors.forename: Yasuhisa
authors.initials: Y
authors.lastname: Iriki
authors.forename: Yuichi
authors.initials: Y
authors.lastname: Ninomiya
authors.forename: Hideki
authors.initials: H
authors.lastname: Okui
authors.forename: So
authors.initials: S
authors.lastname: Kuwahata
authors.forename: Shoji
authors.initials: S
authors.lastname: Fujita
authors.forename: Takehiko
authors.initials: T
authors.lastname: Matsushita
authors.forename: Shiro
authors.initials: S
authors.lastname: Yoshifuku
authors.forename: Ryutaro
authors.initials: R
authors.lastname: Oba
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Hirai
authors.forename: Kinya
authors.initials: K
authors.lastname: Nagata
authors.forename: Chuwa
authors.initials: C
authors.lastname: Tei
mesh_terms: D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000097:blood* / Q000209:etiology; D002097:C-Reactive Protein / Q000032:analysis; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007239:Infections / Q000150:complications*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000737:chemistry*; D010446:Peptide Fragments / Q000097:blood; D011347:Procollagen / Q000097:blood; D051195:Toll-Like Receptor 2 / Q000097:blood*; D015854:Up-Regulation
chemical_list: D015850:Interleukin-6; D010446:Peptide Fragments; D011347:Procollagen; D051195:Toll-Like Receptor 2; C041876:procollagen Type III-N-terminal peptide; D002097:C-Reactive Protein