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Toll-like receptor 2 (TLR2) has recently been shown to be up-regulated in patients with non-valvular atrial fi-brillation (AF). The present study was aimed to determine whether the pathogenesis and development of AF is associated with the up-regulation of TLR2. Clinical data and right atrial appendage (RAA) specimens were col-lected from 20 patients with persisten AF (PeAF), 15 patients with paroxysmal AF (PaAF) and 13 patients with no history of AF undergoing valvular replacement. The results showed that gene expression and protein content of TLR2 were increased in both the AF subgroups, compared with the sinus rhythm (SR) group. Between the two AF subgroups, PaAF had a higher TLR2 level than PeAF. However, no difference in interluekin (IL)-6 content was found among the three groups, and no correlation was found between TLR2 and IL-6 in PeAF patients (r = 0.090, P = 0.706), PaAF patients (r = 0.408, P = 0.131) and AF patients (r = -0.301, P = 0.079). Immunohistochemical analysis revealed that TLR2 was distributed in RAAs of AF patients and confirmed the immunoblotting results. In conclusion, we demonstrated that TLR2 was elevated in AF (especially PaAF) patients with valvular heart disease, further implicating inflammation involved in the pathogenesis and development of AF.
Toll-like receptor 2 (TLR2) has been shown to be up-regulated in patients with non-valvular atrial fi-brillation (AF). The present study was aimed to determine whether the pathogenesis and development of AF is associated with the up -regulation of TLR2. Clinical data and right atrial appendage (RAA) specimens were col-lected from 20 patients with persisten AF (PeAF), 15 patients with paroxysmal AF (PaAF) and 13 patients with no history of AF undergoing valvular replacement. The results showed that gene expression and protein content of TLR2 were increased in both the AF subgroups, compared with the sinus rhythm (SR) group. Between the two AF subgroups, PaAF had a higher TLR2 level than PeAF. However, no difference in interluekin ( IL) -6 content was found among the three groups, and no correlation was found between TLR2 and IL-6 in PeAF patients (r = 0.090, P = 0.706), PaAF patients (r = 0.408, (r = -0.301, P = 0.079). Immunohistochemical analysis revea led that TLR2 was distributed in RAAs of AF patients and confirmed the immunoblotting results. In conclusion, we demonstrated that TLR2 was elevated in AF (especially PaAF) patients with valvular heart disease, further implicating inflammation involved in the pathogenesis and development of AF.