title: NOD2 is highly expressed in Behçet disease with pulmonary manifestations.
abstract: BACKGROUND
  Excessive Th1 cells and TLRs functions are involved in the pathogenesis of Behcet's disease (BD) in response to bacterial antigens. NOD2, an intracellular pathogen recognition sensor, modulates innate defence to muropeptides derived from various bacterial species. To further define a role for NOD2 in BD, we analysed NOD2 transcriptional responses in BAL-MNC from BD patients with pulmonary manifestations.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Histology and Immunology, Department of Basic Sciences, Medicine School of Tunis, Tunis El Manar University, 15 Rue Djebel Lakdar, 1007 Tunis, Tunisia. kamel.hamzaoui@gmail.com.
authors.forename: Kamel
authors.initials: K
authors.lastname: Hamzaoui
authors.forename: Hanadi
authors.initials: H
authors.lastname: Abid
authors.forename: Anissa
authors.initials: A
authors.lastname: Berraies
authors.forename: Jamel
authors.initials: J
authors.lastname: Ammar
authors.forename: Agnès
authors.initials: A
authors.lastname: Hamzaoui