Background Bone marrow mesenchymal stem cells (BM-MSCs) can rejuvenate injured cells through mitochondrial transfer. Our previous study has highlighted the ability of erythropoietin (EPO)-modified BM-MSCs (EPO-BM-MSCs) to relieve asthmatic inflammation. Here, we elucidated whether EPO-BM-MSCs improve asthmatic phenotype by mitochondrial transfer and investigated the underlying mechanism. Methods EPO-BM-MSCs and different modified EPO-BM-MSCs were generated. Ovalbumin (OVA)-induced asthma mouse models were established, and mtCC1-2 cells were treated with CoCl2 to mimic in vitro asthmatic phenotype. EPO-BM-MSC engraftment and mitochondrial transfer from EPO-BM-MSCs to epithelial cells were assessed by fluorescent microscopy and flow cytometry. Mitochondrial membrane potential, ROS production and tunnelling nanotube (TNT) formation were detected by flow cytometry or fluorescent microscopy. Results Intratracheal transplantation of EPO-BM-MSCs alleviated airway inflammation, asthmatic phenotype, and mitochondrial dysfunction in the lungs of OVA-induced asthma mice. Moreover, EPO-BM-MSCs had more efficient effects than BM-MSCs. EPO-BM-MSCs diminished CoCl2-triggered mitochondrial dysfunction in mtCC1-2 cells in vitro, which could be reversed by the inhibitors of TNT formation. When CoCl2-stimulated mtCC1-2 cells were co-cultured with EPO-BM-MSCs,TNT formation significantly increased. EPO-BM-MSCs were validated to donate mitochondria to mtCC1-2 cells through intercellularTNTs in vitro and pulmonary epithelial cells in vivo. EPO-BM-MSCs-upregulated HO-1 contributed to enhanced mitochondrial transfer and improved anti-inflammatory efficacy. Additionally, M-sec promoted intercellular TNT formation and Miro1 enhanced mitochondrial transfer from EPO-BM-MSCsto mtCC1-2 cells. Conclusion Our findings demonstrate that EPO-BM-MSCs rescue epithelial cell injury by mitochondrial donation by upregulating HO-1 to alleviate asthma inflammation, providing novel evidence for the therapeutic potential of EPO-BM-MSCs in asthma.

Pulmonary arterial hypertension (PAH) is a severe pathophysiological syndrome resulting in heart failure, which is found to be induced by pulmonary vascular remodeling mediated by oxidative stress (OS) and inflammation. Phoenixin-20 (PNX-20) is a reproductive peptide first discovered in mice with potential suppressive properties against OS and inflammatory response. Our study will explore the possible therapeutic functions of PHN-20 against PAH for future clinical application. Rats were treated with normal saline, PHN-20 (100 ng/g body weight daily), hypoxia, hypoxia+PHN-20 (100 ng/g body weight daily), respectively. A signally elevated RVSP, mPAP, RV/LV + S, and W%, increased secretion of cytokines, enhanced malondialdehyde (MDA) level, repressed superoxide dismutase (SOD) activity, and activated NLRP3 signaling were observed in hypoxia-stimulated rats, which were notably reversed by PHN-20 administration. Pulmonary microvascular endothelial cells (PMECs) were treated with hypoxia with or without PHN-20 (10 and 20 nM). Marked elevation of inflammatory cytokine secretion, increased MDA level, repressed SOD activity, and activated NLRP3 signaling were observed in hypoxia-stimulated PMECs, accompanied by a downregulation of SIRT1. Furthermore, the repressive effect of PHN-20 on the domains-containing protein 3 (NLRP3) pathway in hypoxia-stimulated PMECs was abrogated by sirtuin1 (SIRT1) knockdown. Collectively, PHN-20 alleviated PAH via inhibiting OS and inflammation by mediating the transcriptional function of SIRT1.

Background:Asthma is an inflammatory disease where the balance between Th1/Th2 and Th17/Treg plays a crucial role in its pathogenesis. Shikonin is used to treat a variety of autoimmune diseases due to its good anti-inflammatory activity. However, the effect and mechanism of shikonin on asthma remain unknown. Method:Mice were sensitized with ovalbumin (OVA)/house dust mite (HDM) and treated with shikonin. Lung inflammation was assessed histologically and via flow cytometry. Bronchoalveolar lavage fluid (BALF) was analyzed for cell counts and cytokines. Shikonin's impact on p-STAT3 was studied in vivo and in vitro. Results:Shikonin inhibited OVA or HDM-induced inflammation and airway hyperresponsiveness. Upon treatment, a restoration of the Th1/Th2 and Th17/Treg balance was observed, evidenced by a reduction in IL-4 and IL-17A levels in BALF, alongside an elevation in interferon-gamma and IL-10. Furthermore, shikonin impeded the infiltration of eosinophils, neutrophils, macrophages, and lymphocytes into lung tissue. The observed decrease in STAT3 phosphorylation and diminished nuclear translocation of p-STAT3 confirmed that shikonin promotes the balance of Th1/Th2 and Th17/Treg by regulating airway epithelial STAT3. Conclusion:Shikonin mitigates asthma symptoms through a STAT3-dependent mechanism, indicating its potential as an anti-asthmatic therapeutic agent.

Abstract Background Homologous recombination deficiency (HRD) is a well‐known biomarker which could predict poly‐ADP ribose polymerase 1 (PARP) inhibitor and platinum drug response. As an aggressive cancer, small‐cell lung cancer (SCLC) is sensitive to platinum drugs, but relapse occurs rapidly. Herein, we aim to illustrate the genomic alteration patterns of homologous recombination repair (HRR)‐related genes in a Chinese SCLC cohort and further analyze the relationship among HRR gene mutations and known biomarkers of immune checkpoint inhibitor (ICI) response, including tumor mutation burden (TMB) and programmed cell death‐ligand 1 (PD‐L1) expression. Methods Next‐generation sequencing (NGS)‐based target capture sequencing of 543 cancer‐related genes was performed to analyze the genomic profiles of 133 Chinese SCLC patients, and TMB was calculated. PD‐L1 expression was evaluated in 90 out of 133 patients using the SP142 PD‐L1 immunohistochemistry assay. Results Among the 133 patients with SCLC, 47 (35.3%) had HRR gene mutations. ATM (8.3%) was the most frequently mutated HRR gene in the cohort, followed by NBN (4.5%). Pathogenic somatic and germline mutations of HRR genes were identified in 11 (23.4%) and 4 (8.5%) patients, respectively. HRR gene mutations cooccurred with KMT2D gene mutations. There were several differences in genomic alterations between patients with HRR gene mutations (HRR‐Mut) and without HRR mutations (HRR‐WT). The results revealed that TP53 and RB1 were commonly mutated genes in both groups. Mutations in the KMT2D gene and genes in the RTK‐RAS pathway occurred more frequently in the HRR‐Mut group. Furthermore, we found that mutations in HRR genes were associated with high TMB (Wilcoxon, p = 0.048), but there was no correlation of HRR gene mutation status with PD‐L1 expression. Conclusions We exhaustively describe the genomic alteration profile of Chinese SCLC patients and provide further evidence that HRR gene mutations are prevalent in SCLC patients.

1 临床资料 患者男性,61岁,主诉"反复咳嗽、咳痰10余年,加重8月余"于2019年4月入住我科.既往史:患者既往体质一般,有煤尘接触史(环卫工人)11年,脱离接触已8年;吸烟20余年,300包/年,已戒烟5年;无其他器官系统疾病.

目的 探讨血清YKL-40水平与肺癌及其合并症患者预后之间的联系.方法 研究共纳入100例肺癌患者,30名健康志愿者作为对照组.记录两组人口学特征,根据合并症分组进行分析,酶联免疫吸附测定(ELISA)血清YKL-40水平.结果 肺癌患者血清YKL-40水平显著高于对照组(P<0.001),而其水平与临床分期、肿瘤大小、有无淋巴结受累和远处转移无关.YKL-40水平高于临界值(133 ng/mL),患者的存活时间显著缩短(P<0.05).YKL-40水平高于临界值合并慢性阻塞性肺疾病(COPD)的患者生存期更短(P<0.05).结论 YKL-40水平可作为肺癌诊断的指标,与肺癌合并COPD患者的预后不良有关.

目的:阐明Notch信号通路对小鼠气道柱状上皮LA-4细胞中Toll样受体4(TLR4)表达的调控作用及其分子机制.方法:观察转染有活性的Notch1胞内段(NIC)对LA-4细胞中TLR4表达的影响;采用双萤光素酶报告基因实验、点突变及染色质免疫沉淀(ChIP)的方法分析Notch/Hes1信号通路对TLR4启动子活性的调控作用.结果:外源性表达NIC可以下调LA-4细胞中TLR4的表达(P<0.05);在小鼠和人TLR4基因转录起始位点上、下游的多个相似位置发现了可能的Hes结合位点N-box;过表达NIC可下调TLR4启动子活性,点突变证实Hes结合位点起到关键作用;ChIP证实LA-4细胞中Hes1结合于TLR4启动子.结论:Notch信号通路可通过Hes1依赖的机制直接调控LA-4细胞中TLR4的表达.

目的 探讨支气管哮喘患者外周血肝X受体(LXRs)、Periostin及蛋白磷酸酶1A(PPM1A)表达与气道重塑间的关系.方法 纳入102例稳定期支气管哮喘患者为哮喘组,同期40例健康志愿者为对照组.收集两组受试者气道壁厚度(T)/气道外径(D)、气道壁面积占气道总横截面面积的百分比(WA％)、血清LXRα、LXRβ、Periostin及PPM1A水平、黏膜下基底膜厚度并比较.采用Pearson相关分析探讨哮喘患者血清LXRα、LXRβ、Periostin及PPM1A水平与T/D、WA％及黏膜下基底膜厚度的关系.结果 哮喘组患者T/D、WA％、血清LXRα、LXRβ、Periostin水平、黏膜下基底膜厚度均明显高于对照组,PPM1A水平明显低于对照组(P<0.05).哮喘患者肺组织HE染色结果提示上皮下基底膜较对照组明显增厚(P<0.05).Pearson相关分析结果显示哮喘患者血清Periostin与T/D、WA％及黏膜下基底膜厚度均呈正相关,血清PPM1A与T/D、WA％及黏膜下基底膜厚度均呈负相关(P<0.05).结论 哮喘患者血清LXRα、LXRβ、Periostin水平异常升高,PPM1A水平异常下降,血清Periostin、PPM1A水平与气道重塑程度存在相关性,可在一定程度上反映哮喘患者的气道重塑情况.

Purpose: N6-methyladenosine (m6A) is among the most abundant mRNA modifications in eukaryote. The aim of the present study was to investigate function of m6A mRNA methylation in lung cancer and the underlying mechanism. Methods: Microarray analysis was performed to detect the differences in RNA expression between cancerous and adjacent non-cancerous tissue samples. The target mRNAs were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Hierarchical clustering of RNAs was conducted to identify distinct m6A methylation or expression patterns between the samples. Results: In the present study, some differentially expressed genes (DEGs) of mRNAs were identified, including up-regulated secret phosphoprotein 1 (SPP1) and down-regulated pRB. Functional enrichment analysis revealed that while differential hypermethylation was related to cell cycle, intracellular part and protein binding, the main pathway involved herpes simplex virus 1 infection related to down-regulated AKT, Araf1 and BCL2A1. In the meantime, sexual reproduction, cohesin complex and protein C-terminus binding was functionally linked to differential hypomethylation, while fluid shear stress and atherosclerosis were identified as the main pathways related to up-regulated GST and CNP. Conclusions: We showed that lung cancer development involved differential expression of SPP1 and pRB mRNA, as well as m6A mRNA methylation in AKT, APAF1, BCL2A1, GST and CNP genes.

目的:探讨外周血T淋巴细胞亚群和基质金属蛋白酶-9(MMP-9)水平在慢性心力衰竭合并肺部感染患者中的变化情况.方法:选择2017年1月-2019年6月空军军医大学第一附属医院治疗的慢性心力衰竭患者360例,根据检查结果分为感染组(156例)和未感染组(204例),比较2组实验室检查指标;多因素logistic回归分析慢性心力衰竭患者合并肺部感染的危险因素;Spearman相关性分析左心室射血分数值(LVEF)、左心室舒张末期内径(LVEDD)、N末端脑钠肽(NT-proBNP)与T淋巴细胞亚群、MMP-9间的相关性;通过受试者工作特征(ROC)曲线探讨T淋巴细胞亚群及MMP-9对评估慢性心力衰竭患者发生肺部感染的最佳临界值.结果:感染组白细胞计数、LVEDD、NT-proBNP、MMP-9水平和CD8+T淋巴细胞比例高于未感染组,而LVEF、CD4+T淋巴细胞比例和CD4+/CD8+比值显著低于未感染组(P 均＜0.05).LVEF＜46.00％、LVEDD≥53.50 mm、NT-proBNP≥580.00 pg/mL、MMP-9≥155.00 pg/L、CD4+T 淋巴细胞＜28.00％、CD8+T 淋巴细胞≥21.00％和 CD4+/CD8+＜1.35为慢性心力衰竭患者合并肺部感染的独立危险因素(P均＜0.05).患者CD4+T淋巴细胞比例及CD4+/CD8+比值与LVEF呈正相关;与LVEDD和NT-proBNP水平呈负相关(P均＜0.05),MMP-9水平和CD8+T淋巴细胞与LVEF呈负相关;与LVEDD和NT-proBNP水平呈正相关(P＜0.05).MMP-9、CD4+/CD8+比值预测慢性心力衰竭患者发生肺部感染的最佳临界值分别为161.27 μg/L、1.41.结论:合并肺部感染的慢性心力衰竭患者免疫功能下降,MMP-9水平升高,T淋巴细胞亚群和MMP-9的水平变化能在一定程度上反映心功能状态和疾病严重程度,并可用作预测肺部感染发生的辅助指标.

目的 探究过表达血红素加氧酶?1(HO?1)的骨髓间充质干细胞(BMSCs)对大鼠急性肺损伤(ALI)的作用及其可能机制.方法 将40只SD大鼠随机分为对照组、模型组、BMSCs?NC组和BMSCs?HO?1组,每组各10只.应用腹腔注射脂多糖(LPS)建立ALI大鼠模型.BMSCs?NC组大鼠尾静脉注射阴性对照BMSCs,BMSCs?HO?1组大鼠尾静脉注射过表达HO?1的BMSCs,其余组大鼠尾静脉注射生理盐水.检测各组大鼠肺泡灌洗液(BALF)中炎症细胞数;采用酶联免疫吸附试验(ELISA)检测BALF中肿瘤坏死因子(TNF)?α、白细胞介素(IL)?6和IL?1β水平.采用苏木素?伊红(HE)染色检测肺组织病理学变化;测定大鼠肺组织湿/干重比(W/D);实时荧光定量聚合酶链反应(qRT?PCR)检测HO?1、表面活性蛋白C(SP?C)mRNA表达水平;蛋白质免疫印迹法(Western blot)检测HO?1、SP?C、NOD样受体热蛋白结构域相关蛋白3(NLRP3)、凋亡相关斑点样蛋白(ASC)和cleaved?Caspase?1蛋白表达水平.结果 与对照组相比,模型组大鼠BALF中细胞总数、中性粒细胞数、巨噬细胞数、TNF?α、IL?6、IL?1β水平、肺损伤评分及W/D均明显升高,肺组织中HO?1和SP?C mRNA、蛋白表达水平均明显降低,NLPR3、ASC和cleaved?Caspase?1蛋白表达水平均明显升高(P<0.05).与模型组相比,BMSCs?NC组大鼠BALF中细胞总数、中性粒细胞数、巨噬细胞数、TNF?α、IL?6、IL?1β水平、肺损伤评分及W/D均明显升高,肺组织中HO?1和SP?C mRNA、蛋白表达水平均明显升高,NLPR3、ASC和cleaved?Caspase?1蛋白表达水平均明显降低(P<0.05).与BMSCs?NC组相比,BMSCs?HO?1组大鼠各项指标均得到进一步改善(P<0.05).结论 过表达HO?1的BMSCs可能通过抑制NLPR3炎症小体活化改善大鼠ALI.

目的 评估慢性阻塞性肺疾病(COPD)患者炎症和氧化应激状态下呼出气冷凝液(EBC)中超细颗粒物(UFP)水平变化.方法 选取2017年6月至2018年12月空军军医大学西京医院收治的符合COPD诊断标准的58例患者为研究对象,另选取同期在该院进行健康体检且无系统性疾病的健康志愿者40例作为对照组.通过常规方法收集EBC,NanoSight纳米颗粒分析仪分析微粒.使用ELISA法测量EBC中羰基和8-羟基脱氧鸟苷(8-OHdG)水平,测定肺活量、肺弥散量.结果 COPD组患者血清嗜酸性粒细胞计数(EOSabs)、C反应蛋白(CRP)及乳酸脱氢酶(LDH)水平均高于对照组(P＜0.05).与对照组相比,COPD组患者EBC中UFP水平降低(P＜0.05),血清中UFP水平升高(P＜0.05),EBC中羰基和8-OHdG水平更高(P＜0.05).EBC中UFP水平与羰基水平呈负相关(P＜0.05),与FEV1和肺一氧化碳扩散能力(DLCO)呈正相关(P＜0.05).EBC中低UFP水平(≤0.18×108/mL)和CRP≥5 mg/L是频繁加重表型的独立预测因子.结论 EBC中UFP水平反映了气道的炎症状态,上皮细胞通透性的增加可能是COPD患者EBC中UFP水平低和血清中UFP水平高的机制.

The present study investigated oxymatrine for anti-proliferative ability against lung cancer cells in vitro and explored related mechanism. Cytotoxicity was assessed by 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT) assay and apoptosis using annexin V-FITC staining. The ROS production was monitored using carboxy-H2-DCFDA and protein expression by western blotting. Oxymatrine at 16 mu M reduced H1975 and A549 cell proliferation to 32.76 and 29.38%, respectively. In oxymatrine treated cells caspase-3 activity and apoptosis was significantly (p < 0.05) increased compared to control. In oxymatrine treated H1975 and A549 cells a marked promotion in p-p38 and p-JNK1/2 protein level and suppression of p-ERK 1/2 level was observed. Exposure of H1975 and A549 cells to PD169316 (p38 inhibitor) and SP600125 (JNK inhibitor) at 5 mM doses significantly alleviated oxymatrine (16 FM) mediated elevation of caspase-3 activity. Production of ROS was much higher in oxymatrine treated H1975 and A549 cells compared to control cells. The oxymatrine mediated ROS production up-regulation was inhibited in H1975 and A549 cells on pre-treatment with NAC. In FeTMPyP-pretreated cells increase in p-p38 and p-JNK expression by oxymatrine (16 mu M) was completely alleviated. Thus oxymatrine inhibits lung cancer proliferation in vivo by oxidative response induced cell apoptosis. The p38/JNK activation was promoted and ERK 1/2 phosphorylation inhibited by oxymatrine in H1975 and A549 cancer cells. Therefore, oxymatrine has anti-proliferative activity against lung cancer cells which needs to be studied using in vivo studies.

目的:盐酸氨溴索对烟所致慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)大鼠肺组织细胞凋亡和血管重塑的作用机制研究.方法:将SD大鼠随机分为4组,每组20只,依次为正常组、模型组、实验组、对照组.模型组、实验组、对照组大鼠采延安香烟烟熏64天构建慢性阻塞性肺大鼠模型,正常组大鼠室温下正常饲养.烟熏结束后,实验组、对照组大鼠每日分别皮下注射5ml盐酸氨溴索(20 mg/kg)和5mL的盐酸班布特罗(20 mg/kg),正常组、模型组分别腹腔注射等剂量的生理盐水.在药物干预28天后,苏木精-伊红染色(hematoxylin-eosinstaining,HE)、弹力纤维(elastic van gieson,EVG)染色、TUNNEL染色、免疫组化染色、Western blot检测各组大鼠肺组织病理、血管重塑、肺组织的细胞凋亡、α-平滑肌肌动蛋白(α-smoothmus-cleactin,α-SMA)和血管内皮生长因子(Vascular endothelial growth factor,VEGF)的表达、以及Caspase-3、Bax和Bcl-2的表达水平.结果:与正常组相比,模型组肺组织损伤明显,肺小动脉中膜厚度明显增加,血管肌化程度、细胞的凋亡率、α-SMA和VEGF、Cas-pase-3、Bax的表达明显升高,Bcl-2的表达明显降低,差异均具有统计学意义(P＜0.05);与模型组相比,实验组和对照组大鼠肺组织损伤明显改善,肺小动脉中膜厚度明显减小,血管肌化程度、细胞的凋亡率、α-SMA和VEGF、Caspase-3、Bax的表达明显降低,Bcl-2的表达明显升高,差异均具有统计学意义(P＜0.05).结论:盐酸氨溴索能抑制肺组织的细胞凋亡以及改善其血管重塑,保护COPD大鼠的肺组织.

An increasing number of studies have demonstrated that phillygenin (PG) exerts anti-oxidant, anti-inflammatory and anti-cancer activities. However, the effects of PG on the proliferation and invasion in non-small cell lung cancer (NSCLC) cells have not been clarified. In this study, MTT assay and flow cytometry were conducted to investigate the effect of PG on proliferation and apoptosis of NSCLC cells in vitro, respectively. A xenograft model of A549 cell was established in nude mice to validate the in vitro findings. Western blot were performed to measure the expression of molecules involved in AMPK/ERK/NF-κB pathway. Results suggested that PG (50 or 100 μM) was significantly cytotoxic to A549 cells and SPC-A1 cells in vitro. PG treatment also inhibited the tumor growth of NSCLC cell mouse xenografts in vivo. These anti-proliferative and pro-apoptosis effects of PG were found to be regulated by the AMPK/ERK/NF-κB pathway. Consequently, PG suppressed proliferation and induced cell apoptosis in NSCLC cells. In conclusions, PG regulates AMPK/ERK/NF-κB axis in NSCLC cells, thereby inhibiting the proliferation and promoting the apoptosis of NSCLC cells.

目的 探讨陕西地区高龄COPD(慢性阻塞性肺病)伴肺部感染人群ABA(鲍氏不动杆菌)的分布特征及影响患者预后的因素.方法 回顾性研究2015年01月至2019年11月西安国际医学中心医院及陕西省人民医院收治的1078例高龄COPD患者,分为ABA感染组63例与非ABA感染组1015例.通过电子病历系统,收集患者基本信息,对比两组患者预后结局.患者基线资料采用单因素分析,差异有统计学意义的单因素采用Logistic分析.结果 感染组病死率[12.70％(8/63)]明显高于非感染组[4.43％(45/1015)](χ2=8.670,P=0.003).两组在年龄、APACHE II评分、糖尿病、PCT及ICU住院时间方面差异有统计学意义(P<0.05).感染组存活患者55例,好转出院42例,需延长住院13例,死亡8例.Logistic回归分析表明,APACHE II评分(OR=3.480,95％CI:1.154～10.491)、糖尿病(OR=2.732,95％CI:1.297～5.753)、血清高水平PCT(OR=6.334,95％CI:1.142～35.129)及ICU住院时间(OR=3.773,95％CI:1.087～13.100)是影响患者预后的独立危险因素.结论 ABA 感染与年患者龄、APACHE II评分、糖尿病、PCT及ICU住院时间相关,APACHE II评分、糖尿病、PCT及ICU住院时间影响患者预后.

目的 探讨程序性死亡配体1(PD-L1)在接受抗癌治疗的非小细胞肺癌(NSCLC)患者组织中的表达变化.方法 收集空军军医大学西京医院呼吸内科76例NSCLC患者的临床信息及组织标本,通过免疫组化(IHC)评估患者接受抗癌治疗前后PD-L1的表达,分析PD-L1表达与生存结果的关系.结果 43％的NSCLC患者在接受抗癌治疗后,肿瘤组织标本中的PD-L1的表达发生变化,且与接受非全身性抗癌治疗患者相比,接受表皮生长因子受体酪氨酸激酶抑制剂(EGFR TKI)治疗患者的PD-L1表达显著增加(P=0.031).与此同时,预后分析显示,PD-L1阳性表达和阴性表达对患者的预后没有显著性影响(P=0.065).结论 在接受抗癌治疗后,部分NSCLC患者的肿瘤组织标本的PD-L1的表达会发生变化,且EGFR-TKI治疗显著促进了NSCLC患者的PD-L1表达,这为PD-L1在NSCLC中的治疗提供了理论基础.

目的:探讨胸腔积液结核分枝杆菌感染T细胞检测(T-SPOT.TB)对结核性胸膜炎的诊断价值.方法:选择75例胸腔积液患者为研究对象,其中结核性胸膜炎患者52例(结核组),非结核性胸膜炎患者23例(非结核组).比较两组患者胸腔积液T-SPOT.TB、腺苷脱氨酶(ADA)及外周血T-SPOT.TB水平.通过受试者工作特征(ROC)曲线分析胸腔积液T-SPOT.TB、ADA及外周血T-SPOT.TB对结核性胸膜炎的诊断效能.结果:两组患者胸腔积液T-SPOT.TB、ADA及外周血T-SPOT.TB比较,差异均具有统计学意义(P<0.05).在诊断结核性胸膜炎方面,胸腔积液T-SPOT.TB表现出较高的敏感度及特异度.结论:与其他检测指标相比,胸腔积液T-SPOT.TB的灵敏度和特异度较高,可以提高诊断的准确率.

Objective:To investigate the effects of bronchoalveolar lavage on the surface active protein A (SPA) and high mobility protein 1 (HMGA1) of patients with pulmonary abscess.Methods:A retrospective, random sampling method was performed in 120 cases of patients with pulmonary abscess in our hospital from February 2014 to June 2017, they were divided into the observation group and the control group by different treatment methods with 60 patients in each group.The control group was given routine treatment, the observation group was given bronchoalveolar lavage therapy based on the treatment of control group, all patients were observed for 4weeks.The clinical efficacy, changes in lung function, serum SPA and HMGA1 levels before and after treatment were compared between the two groups.Results:The total effective rate in the observation group (98.3％) was significantly higher than that in the control group (88.3％) (P＜0.05).The FEV1 and PaO2after treatment in both groups were significantly increased than those before treatment (P＜0.05), and the above indicators of observation group were significantly higher than those in the control group (P＜0.05).The serum SPA and HMGA1 levels after treatment in both groups were significantly lower than those before treatment (P＜0.05), and the above indicators of observation group were significantly lower than those in control group (P＜0.05).Conclusions:Bronchoalveolar lavage can effectively enhance the clinical therapeutic effect of pulmonary abscess, significantly improve the pulmonary function and blood gas status of patients, and its mechanism may be related to the reduction of serum SPA and HMGA1 levels of patients.

Objective: To investigate the relationship between IFNL4 expression and macrophage functions, analyze the role of IFNL4 in immune regulation, and explore for the potential application value of IFNL4 in immune regulation. Methods: The THP-1 cell culture and stimulation system was esteblished. The IFNL4 expressions in different type of THP-1 cells were detected by RT-PCR.IFNL4 was then overexpressed in THP-1 cells, and the expression of IL-12, TNF-α, IL-10 and TGF-β in these cells were analyzed by RT-PCR. The migration efficiency of THP-1 cells was analyzed by transwell assay before or after IFNL4 overexpression. Results: The differentiation of THP-1 cells inhibited IFNL4 expression (P ＜0.001), and M2 macrophage can secrete more IFNL4 comparing to M1 macrophage (P=0.009). IFNL4 overexpression in THP-1 cells inhibit IL-12 and TNF-α secretion while promote IL-10 and TGF-βexpression, in which TNF-α and TGF-β variations were significantly different (P=0.017 and p=0.046, respectively). Furthermore, IFNL4 overexpression inhibit THP-1 cell migration significantly (P=0.005). Conclusion: IFNL4 has a certain inhibitory effect on inflammation function of macrophage in THP-1 cell system.