Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:Mechanical ventilation modulates TLR4 and IRAK-3 in a non-infectious, ventilator-induced lung injury model. | Villar et al. Respiratory Research 2010 11 27 http content 11 1 27 RESPIRATORY RESEARCH RESEARCH Open Access Mechanical ventilation modulates TLR4 and IRAK-3 in a non-infectious ventilator-induced lung injury model Jesus Villar1 2 3 3 Nuria E Cabrera1 23 Milena Casula1 2 Carlos Flores1 43 Francisco Valladares1 5 Lucio Diaz-Flores5 Mercedes Muros1 6 Arthur S Slutsky3 7 8 Robert M Kacmarek9 10 Abstract Background Previous experimental studies have shown that injurious mechanical ventilation has a direct effect on pulmonary and systemic immune responses. How these responses are propagated or attenuated is a matter of speculation. The goal of this study was to determine the contribution of mechanical ventilation in the regulation of Toll-like receptor TLR signaling and interleukin-1 receptor associated kinase-3 IRAK-3 during experimental ventilator-induced lung injury. Methods Prospective randomized controlled animal study using male healthy adults Sprague-Dawley rats weighing 300-350 g. Animals were anesthetized and randomized to spontaneous breathing and to two different mechanical ventilation strategies for 4 hours high tidal volume VT 20 ml kg and low VT 6 ml kg . Histological evaluation TLR2 TLR4 IRAK3 gene expression IRAK-3 protein levels inhibitory kappa B alpha IftBa tumor necrosis factor-alpha TNF-a and interleukin-6 IL6 gene expression in the lungs and TNF-a and IL-6 protein serum concentrations were analyzed. Results High VT mechanical ventilation for 4 hours was associated with a significant increase of TLR4 but not TLR2 a significant decrease of IRAK3 lung gene expression and protein levels a significant decrease of IftBa and a higher lung expression and serum concentrations of pro-inflammatory cytokines. Conclusions The current study supports an interaction between TLR4 and IRAK-3 signaling pathway for the overexpression and release of pro-inflammatory cytokines during ventilator-induced lung injury. Our study also suggests that .