Sepsis is a pathological condition in which the body’s response to infection is dysfunctional and may lead to life-threatening organ failures as one of the leading causes of death worldwide. However，there is still a lack of effective prevention and treatment for sepsis. IL-17A is an inflammatory cytokine produced primarily by activated T cells and is involved in host defense，tissue repair，the pathogenesis of inflammatory diseases，and the progression of cancer. This article reviews the recent research progress on the roles of IL-17A in sepsis-related organ damage，and its potentials as a novel therapeutic target for the clinical treatment of sepsis.

Objective To assess the health status of rodent laboratory animals by pathological diagnosis, our lab has being take apart in investigating the quality of laboratory animals in Beijing area for years and offer some advices for standardized breeding to ensure accurate results of scientific research.This paper focuses on the analysis of laboratory rodent samples that collected in October 2014.Methods We collected the heart, liver, spleen, lung, kidney, large intestine and small intestine, and put these organs into 10%Calcium formaldehyde solution for fixation, and then prepared into two different sections for optical microscopy observation including all paraffin specimens stained with H&E and the frozen sections stained with Oil Red-O and PAS.Results The vast majority of laboratory rodents were up to standard, but there still a problem in individual units.The main problem is liver and lung disease.The rate of Hepatocyte swellingis 6%(mouse), 2.5% (rat), 8.2% (guinea pig), moreover part of them were lipidosis, according to Oil Red-O stain.the mainly problem of lung is congestion ,edema and Interstitial pneumonia ,the detectable rate of pulmonarydiseases is 15.5%(guinea pig).Conclusions The vast majority of laboratory rodents were pathologically diagnosed as healthy animals.The liver disease may be caused by improper feeding.And disease of lung may led by haze, unqualified bedding and low temperature.

Objective:To explore the dynamic phenotype of type Ⅱ alveolar epithelial cells(AEC Ⅱ)in radiation-induced lung fibrosisand its role in the formation of fibrosis.Methods:Totally 90 C57BL/6J female mice were divided into 2 groups: irradiation group (50, thoracic irradiation with a single dose of 20 Gy X-rays), control group (40, sham irradiation). At 24 h, 4 and 12 weeks after irradiation, 5 mice were euthanized and the lungs were collected for pathological observation. The other lungtissues were collected for the isolation of primary AEC Ⅱ cells with microbeadssorting.The mRNA expressions of proSP-C, HOPX, vimentin, β-catenin and TGF-β1 in AEC II cells were detected by RT-PCR.Results:Acute pneumonitis was observed in the lungs at 24 h after irradiation and alleviated in accompany with partial alveolar septal thickening and a small amount of collagen deposition at 4 weeks after irradiation. The collagen deposition became more pronounced at 12 weeks after irradiation, together with collapsed and fused alveolar cavities, alveolar septal hyperplasia, and pulmonary fibrosis formation.The mRNAexpression levels of proSP-C and HOPX in primary AEC Ⅱ cells increased at 24 hours after irradiation and then approached to a peak value at 4 weeks after irradiation ( F=8.441, 3.586, P=0.036). The mRNA expression levels of vimentin, a biomarker of EMT, was increased significantly at 4 weeks and continued up to 12 weeks after irradiation( F=8.358, P=0.001). The mRNA expression levels of profibrotic factors β-catenin and TGF-β1 were both significant increased at 12 weeks after irradiation( F=4.62, 3.279, P=0.044). Conclusions:The phenotypeof AECⅡ cells could not only be transformed from proSP-C+ to HOPX+ /proSP-C+ , HOPX+ /proSP-C+ /vimentin+ , and vimentin+ /proSP-C, but also differentiated into mesenchymal cells with highly expressed profibrotic factors, thereby inducing EMT process, which either played a role in the repair of radiation-induced lung injury or triggered radiation-induced fibrosis.