Clinical scientists have paid more and more attention to the acute respiratory distress syndrome(ARDS), a severe complication after thoracotomy, for its high mortality rate. Compared with other surgical patients, patients who received thoracotomy often have a worse cardiopulmonary function and are prone to suffering from ARDS. Surgical treatment or injury, massive blood transfusion, respiratory tract infection, improper fluid replacement and ventilation are probable reasons to cause ARDS. Mechanical ventilation is an important treatment for ARDS，but ventilation with lungprotective strategies was proved to be the only therapy which can improve the prognosis of patients with ARDS. At present, thinking highly of and promoting the perioperative management, lessening surgical injury and active prevention are still very important measures to reduce the mortality after thoracotomy. This article is aimed to review the high risk factors of ARDS after thoracotomy as well as its treatment.
Objective To identify the effects of single immunoglobin IL-1 receptor related protein （SIGIRR） on inflammation induced by high mobility group box 1 （HMGB1） in A549 derived from human alveolar epithelial cells. Methods Eukaryotic expression vectors pCDNA3.1（+） constructed with SIGIRR cDNA were transiently transfected into A549 cells，in which SIGIRR was forced to be over-expressed. Western blot and RT-PCR were applied to detect the expression level of SIGIRR after transfection. After the stimulation by HMGB1，the transcriptional activity of NF-κB in A549 cells was detected by dual-luciferase reporter assay system，and the protein levels of inflammatory cytokine TNF-α and IL-1β were measured by ELISA. Results The expression level of SIGIRR increased significantly in A549 cells transfected with SIGIRR vectors. The transcriptional activity of NF-κB was enhanced obviously after HMGB1 treatment in A549 cells by dual-luciferase reporter assay system，while the transfection of SIGIRR vectors decreased the activity. The protein levels of TNF-α and IL-1β were down-regulated in A549 cells over-expressing SIGIRR after HMGB1 stimulation compared with the non-transfected cells. Conclusions Up-regulated SIGIRR expression can inhibit HMGB1-induced proinlammatory cytokine release in A549 cells such as TNF-α and IL-1β. The transcriptional activity of NF-κB is dampened by SIGIRR transfection，implying that the anti-inflammatory effects of SIGIRR may be involved in the regulation of NF-κB.
Objective To detect the expression of single immunoglobin IL-1 receptor related protein ( SIGIRR) in normal human lung tissues, and study its changes in alveolar epithelial cell acutely injured by lipopolysaccharide ( LPS) . Methods Twenty samples of human normal lung tissue were collected during the lobectomies. The expression of SIGIRR was detected by immunohistochemistry, western blot and RT-PCR. The human type II alveolar epithelial cell acute injury model was established by stimulating A549 cells with LPS of a final concentration of 10 μg/mL. The cells were collected at 0, 3, 6, 12, and 24 hours after the stimulation. The changes of SIGIRR expression at the same time points were observed by western blot. The expression vector containing full-length SIGIRR cDNA was transfected transiently into A549 cells to induce SIGIRR overexpression. MTT assay was performed to measure the injury of A549 cells caused by LPS. Results The immunohistochemistry, western blot and RT-PCR showed that there was a high expression of SIGIRR in normal human lung tissues. The expression of SIGIRR was located in alveolar epithelial cells by immunohistochemistry. The expression of SIGIRR at 3, 6, and 12 hours was down-regulated after LPSstimulation and raised again at 24 hours to the baseline. MTT assay showed that SIGIRR overexpression substantially reduced the growth inhibition ratio of A549 cells after LPS stimulation. Conclusions Expression of SIGIRR in normal human lung tissues was confirmed by different detection methods. SIGIRR alleviates the injury of alveolar epithelial cells caused by LPS, implying SIGIRR might be involved in the regulationof acute lung injury mediated by LPS.