TLR2 was overexpressed independent of IL-6 in patients with valvular atrial fibrillation

Jian Wang,Lei Xue,Hailong Cao,Fei Cui,Ting Dai,Yijiang Chen

doi:10.1016/s1674-8301(11)60023-7

Jian Wang, Lei Xue + Show 4 more

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https://doi.org/10.1016/s1674-8301(11)60023-7

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Abstract

Toll-like receptor 2 (TLR2) has recently been shown to be up-regulated in patients with non-valvular atrial fibrillation (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 collected 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.

Highlights

Atrial fibrillation (AF), the most common arrhythmia seen in clinical practice[1], is associated with substantial morbidity and mortality
Toll-like receptor 2 (TLR2) could be detected in the right atrial appendage (RAA) tissues of AF and sinus rhythm (SR) patients with valvular heart disease
The mRNA transcripts of TLR2 were elevated in patients with paroxysmal AF (PaAF) and persisten AF (PeAF), compared with those in patients with SR (Fig. 1)

Summary

Introduction

Atrial fibrillation (AF), the most common arrhythmia seen in clinical practice[1], is associated with substantial morbidity and mortality. AF is generally categorized into valvular and non-valvular AF, depending on the presence of valvular heart disease. Various disorders, such as ischemic, valvular, inflammatory and degenerative heart diseases, as well as hormonal disorders and systemic hypertension, predispose to AF . A number of risk factors have been associated with AF, acute or chronic hemodynamic, metabolic, and especially inflammatory stressors may lead to structural remodeling of the atria that may promote progression and persistence of AF. Serum markers have been measured to assess the involvement of systemic inflammation in the initiation and promotion of AF and the development of cardioembolic stroke

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