为探讨急性呼吸窘迫综合征肺泡炎症中IL-17A的表达及意义,选择急性呼吸窘迫综合征肺泡炎症患者98例,根据病情严重程度分为A组(轻度,36例)、B组(中度,32例)及C组(重度,30例),均进行IL-17A水平及中性粒细胞计数检测,比较3组患者血清IL-17...为探讨急性呼吸窘迫综合征肺泡炎症中IL-17A的表达及意义,选择急性呼吸窘迫综合征肺泡炎症患者98例,根据病情严重程度分为A组(轻度,36例)、B组(中度,32例)及C组(重度,30例),均进行IL-17A水平及中性粒细胞计数检测,比较3组患者血清IL-17A水平、中性粒细胞计数、急性生理学与慢性健康状况评分系统Ⅱ(acute physiology and chronic health evaluation scoring systemⅡ,APACHEⅡ)评分、序贯器官功能衰竭(sequential organ failure assessment,SOFA)评分及治疗前后血清IL-17A水平,分析不同预后患者血清IL-17A水平及其价值。结果显示,C组患者血清IL-17A水平、中性粒细胞计数、APACHEⅡ评分及SOFA评分均高于A组和B组,且B组高于A组(P<0.05);3组患者治疗后血清IL-17A水平均低于治疗前,但C组血清IL-17A水平仍高于A组和B组,且B组高于A组(P<0.05);经Pearson分析,IL-17A水平与APACHEⅡ评分、SOFA评分呈正相关(P<0.05);经28 d随访,98例患者中存活60例,死亡38例,存活者血清IL-17A水平明显低于死亡者(P<0.05);经受试者工作特征(receiver operating characteristic,ROC)曲线分析,AUC为0.859。研究提示,急性呼吸窘迫综合征肺泡炎症患者IL-17A的表达水平升高,动态监测IL-17A水平可判断病情进展及预后。展开更多
CD1d-restricted natural killer T(NKT)cells are innate-like T lymphocytes with protective or pathogenic roles in the development of influenza pneumonia.Here,we show that lung-infiltrated and activated NKT cells are the...CD1d-restricted natural killer T(NKT)cells are innate-like T lymphocytes with protective or pathogenic roles in the development of influenza pneumonia.Here,we show that lung-infiltrated and activated NKT cells are the major cellular source of LIGHT/TNFSF14,which determines the severity of pulmonary pneumonia by highly deteriorative influenza A virus(IAV)infection.Compared to wild-type mice,LIGHT^(-/-)mice exhibit much lower morbidity and mortality to IAV,due to alleviated lung damage and reduced apoptosis of alveolar macrophages(AMs).LIGHT preferentially promotes cell death of lymphotoxin β receptors positive(LTβR^(+))AMs but not herpesvirus entry mediator positive(HVEM^(+))AMs.Therefore,these results suggest that NKT-derived LIGHT augments cell death of the tissue protective AMs in exacerbating lung pathology and susceptibility to fatal influenza infection.Suppression of LIGHT signaling might be a viable option in the treatment of influenza-associated acute respiratory distress syndrome.展开更多
OBJECTIVE: To assess the effect of Tanreqing injection on airway inflammation in rats. METHODS: A rat model of airway inflammation was generated with lipopolysaccharide (LPS). Tanreqing injection was given by intratra...OBJECTIVE: To assess the effect of Tanreqing injection on airway inflammation in rats. METHODS: A rat model of airway inflammation was generated with lipopolysaccharide (LPS). Tanreqing injection was given by intratracheal instillation, and bronchoalveolar lavage fluid (BALF) from the right lung was collected. BALF total cell and neutrophil counts were then determined. In addition, BALF levels of inflammatory cytokines interleukin-1β, cytokine-induced neutrophil chemoattractant-1, and tumor necrosis factor-α were measured using enzyme linked immunosorbent assay.The middle lobe of the right lung was stained with hematoxylin-eosin and histological changes examined. RESULTS: LPS increased airway inflammation, decreased BALF inflammatory cell count, inflammatory cytokine levels, and suppressed leukocyte influx of the lung. The LPS-induced airway inflammation peaked at 24 h, decreased beginning at 48 h, and had decreased markedly by 96 h. CONCLUSION: Tanreqing injection contains anti-inflammatory properties, and inhibits airway inflammation in a dose-dependent manner.展开更多
This study aimed to establish an animal model of decompression-induced lung injury(DILI)secondary to repetitive diving in mice and explore the role of macrophages in DILI and the protective effects of high-concentrati...This study aimed to establish an animal model of decompression-induced lung injury(DILI)secondary to repetitive diving in mice and explore the role of macrophages in DILI and the protective effects of high-concentration hydrogen(HCH)on DILI.Mice were divided into three groups:control group,DILI group,and HCH group.Mice were exposed to hyperbaric air at 600 k Pa for 60 min once daily for consecutive 3 d and then experienced decompression.In HCH group,mice were administered with HCH(66.7%hydrogen and 33.3%oxygen)for 60 min after each hyperbaric exposure.Pulmonary function tests were done 6 h after decompression;the blood was harvested for cell counting;the lung tissues were harvested for the detection of inflammatory cytokines,hematoxylin and eosin(HE)staining,and immunohistochemistry;western blotting and polymerase chain reaction(PCR)were done for the detection of markers for M1 and M2 macrophages.Our results showed that bubbles formed after decompression and repeated hyperbaric exposures significantly reduced the total lung volume and functional residual volume.Moreover,repetitive diving dramatically increased proinflammatory factors and increased the markers of both M1 and M2 macrophages.HCH inhalation improved lung function to a certain extent,and significantly reduced the pro-inflammatory factors.These effects were related to the reduction of M1 macrophages as well as the increase in M2 macrophages.This study indicates that repetitive diving damages lung function and activates lung macrophages,resulting in lung inflammation.HCH inhalation after each diving may be a promising strategy for the prevention of DILI.展开更多
文摘为探讨急性呼吸窘迫综合征肺泡炎症中IL-17A的表达及意义,选择急性呼吸窘迫综合征肺泡炎症患者98例,根据病情严重程度分为A组(轻度,36例)、B组(中度,32例)及C组(重度,30例),均进行IL-17A水平及中性粒细胞计数检测,比较3组患者血清IL-17A水平、中性粒细胞计数、急性生理学与慢性健康状况评分系统Ⅱ(acute physiology and chronic health evaluation scoring systemⅡ,APACHEⅡ)评分、序贯器官功能衰竭(sequential organ failure assessment,SOFA)评分及治疗前后血清IL-17A水平,分析不同预后患者血清IL-17A水平及其价值。结果显示,C组患者血清IL-17A水平、中性粒细胞计数、APACHEⅡ评分及SOFA评分均高于A组和B组,且B组高于A组(P<0.05);3组患者治疗后血清IL-17A水平均低于治疗前,但C组血清IL-17A水平仍高于A组和B组,且B组高于A组(P<0.05);经Pearson分析,IL-17A水平与APACHEⅡ评分、SOFA评分呈正相关(P<0.05);经28 d随访,98例患者中存活60例,死亡38例,存活者血清IL-17A水平明显低于死亡者(P<0.05);经受试者工作特征(receiver operating characteristic,ROC)曲线分析,AUC为0.859。研究提示,急性呼吸窘迫综合征肺泡炎症患者IL-17A的表达水平升高,动态监测IL-17A水平可判断病情进展及预后。
基金supported by the Chinese Academy of Sciences(XDB29030301)the Ministry of Science and Technology(2018ZX10101004002004 and 2018YFC1200703)the National Natural Science Foundation of China(31321001,31621061,81590764,and 31400755)。
文摘CD1d-restricted natural killer T(NKT)cells are innate-like T lymphocytes with protective or pathogenic roles in the development of influenza pneumonia.Here,we show that lung-infiltrated and activated NKT cells are the major cellular source of LIGHT/TNFSF14,which determines the severity of pulmonary pneumonia by highly deteriorative influenza A virus(IAV)infection.Compared to wild-type mice,LIGHT^(-/-)mice exhibit much lower morbidity and mortality to IAV,due to alleviated lung damage and reduced apoptosis of alveolar macrophages(AMs).LIGHT preferentially promotes cell death of lymphotoxin β receptors positive(LTβR^(+))AMs but not herpesvirus entry mediator positive(HVEM^(+))AMs.Therefore,these results suggest that NKT-derived LIGHT augments cell death of the tissue protective AMs in exacerbating lung pathology and susceptibility to fatal influenza infection.Suppression of LIGHT signaling might be a viable option in the treatment of influenza-associated acute respiratory distress syndrome.
基金Supported by the Program for Innovative Research at the West China School of Medicine, Sichuan University, and Sichuan Technology Department (No. 2012SZ0288)
文摘OBJECTIVE: To assess the effect of Tanreqing injection on airway inflammation in rats. METHODS: A rat model of airway inflammation was generated with lipopolysaccharide (LPS). Tanreqing injection was given by intratracheal instillation, and bronchoalveolar lavage fluid (BALF) from the right lung was collected. BALF total cell and neutrophil counts were then determined. In addition, BALF levels of inflammatory cytokines interleukin-1β, cytokine-induced neutrophil chemoattractant-1, and tumor necrosis factor-α were measured using enzyme linked immunosorbent assay.The middle lobe of the right lung was stained with hematoxylin-eosin and histological changes examined. RESULTS: LPS increased airway inflammation, decreased BALF inflammatory cell count, inflammatory cytokine levels, and suppressed leukocyte influx of the lung. The LPS-induced airway inflammation peaked at 24 h, decreased beginning at 48 h, and had decreased markedly by 96 h. CONCLUSION: Tanreqing injection contains anti-inflammatory properties, and inhibits airway inflammation in a dose-dependent manner.
基金Project supported by the National Natural Science Foundation of China(No.81772015)。
文摘This study aimed to establish an animal model of decompression-induced lung injury(DILI)secondary to repetitive diving in mice and explore the role of macrophages in DILI and the protective effects of high-concentration hydrogen(HCH)on DILI.Mice were divided into three groups:control group,DILI group,and HCH group.Mice were exposed to hyperbaric air at 600 k Pa for 60 min once daily for consecutive 3 d and then experienced decompression.In HCH group,mice were administered with HCH(66.7%hydrogen and 33.3%oxygen)for 60 min after each hyperbaric exposure.Pulmonary function tests were done 6 h after decompression;the blood was harvested for cell counting;the lung tissues were harvested for the detection of inflammatory cytokines,hematoxylin and eosin(HE)staining,and immunohistochemistry;western blotting and polymerase chain reaction(PCR)were done for the detection of markers for M1 and M2 macrophages.Our results showed that bubbles formed after decompression and repeated hyperbaric exposures significantly reduced the total lung volume and functional residual volume.Moreover,repetitive diving dramatically increased proinflammatory factors and increased the markers of both M1 and M2 macrophages.HCH inhalation improved lung function to a certain extent,and significantly reduced the pro-inflammatory factors.These effects were related to the reduction of M1 macrophages as well as the increase in M2 macrophages.This study indicates that repetitive diving damages lung function and activates lung macrophages,resulting in lung inflammation.HCH inhalation after each diving may be a promising strategy for the prevention of DILI.
