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NOD2 is highly expressed in Beh?et disease with pulmonary manifestations

DOI: 10.1186/1476-9255-9-3

Keywords: NOD2, TLRs, T-bet, Beh?et Disease, Inflammation

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We analysed NOD1, NOD2, T-bet and TLRs mRNA expression with real-time polymerase chain-reaction in BAL cells obtained from 23 BD patients with pulmonary manifestations and their matched controls.We found that NOD2 mRNA expression was highly up-regulated in BAL cells from BD and sarcoidosis patients compared to healthy control group (P = 0.001). In BD patients, significant correlation was found between NOD2 and T-bet mRNA expression (r = 0.602; P = 0.0009). In BAL from BD patients, NOD2 and T-bet mRNA expression were significantly correlated with BAL-lymphocytes (r = 0.485, P = 0.010; r = 0684, P = 0.0001 respectively). NOD2 in BD was also correlated with TLR 2(r = 0.444; P = 0.021) and TLR 4 (r = 0.574; P = 0.001) mRNA expression.Our results indicate that BAL-MNC from BD patients expressed NOD2 as a result of lung inflammation. TLRs and NOD2 synergize for the induction of proinflammatory cytokines. BAL inflammatory cells showed an increased Th1 situation as indicated by increased T-bet mRNA expression.Behcet's disease (BD) is a systemic vasculitis with unknown aetiology. Immune dysregulation involving T and B cells with hyperreactive neutrophils, supposedly triggered by infectious agents, contribute to disease pathogenesis in addition to genetic predisposition [1-3]. Documentation of various atypical streptococcal species in oral flora of BD patients, clinical flares after dental procedures, and a good response to antibacterial treatment, have been considered as evidence for the role of Streptococcus in BD [4]. However, none of the microbial agents has been definitely proved to cause BD. Immunological disorders are important in BD pathogenesis [5]. T lymphocytes from patients with BD produced a particular inflammatory mediators pattern when stimulated with a bacterial superantigen [6-9]. Innate immunity was deeply investigated in BD patients [9,10]. Toll-like receptor (TLR)-expressing cells (TLR-2 and TLR-4) [9] and gamma delta T cells (TCRγδ) [11] have been involve


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