慢性阻塞性肺疾病(COPD)是一种具有气流受限特征的疾病，气流受限不完全可逆，呈进行性发展，其发病与肺部对有害气体或有害颗粒尤其是吸炯引起的异常炎症反应有关。一般来说，40岁以上的患者，如果过去或现在还在吸炯 有咳嗽、咳痰或气紧，就应考虑COPD可能。COPD的诊断与病情程度分级一般取决于肺功能检测所反映的气流受限程度，但是有越来越多的证据显示COPD的临床表现与气流受限程度不完全相关[1] 。因此，为了对COPD有一个全面系统的认识，还需要同时评估影像学表现、运动耐力和体重指数(BMI)。正是基于此项认识，有作者[2]认为COPD不能仅仅理解为一种肺部的慢性疾病，COPD患者常伴有全身多个系统的慢性病变，它可能是一种慢性全身性炎症综合征(chronic systemic inflammatory syndrome)o如有多个研究发现COPD可能伴有某种程度的全身炎症反应[3,4]，Gan等[5]通过荟萃分析认为，即使在稳定期COPD也有外周血中性粒细胞(尤其是活化的表型)增多、急性相反应蛋白(C反应蛋白和纤维蛋白原)、白细胞介素6(IL-6)和肿瘤坏死因子α(TNF-α)水平增加。有趣的是，其他慢性疾病如慢性心力衰竭、肥胖、糖尿病甚至正常的老龄化也有同样程度的全身炎症反应 。
Objective Bone marrow mesenchymal stem cells （MSCs） have been suggested to play an important role in the treatment of a variety of pulmonary diseases. The present study was aimed at evaluating the therapeutical effect of MSCs transplantation on emphysematous rats，and explore its influence in local and systemic inflammation. Methods Emphysema rat model was established by cigarette smoking. MSCs were transfected with lentivirus vector carrying green fluorecent protein （GFP） and the transfected MSCs in lung of smoke rats were detected by imaging system for small animals. Thirty-six SD rats were randomly divided into a control group，an emphysema group，and a MSCs transplantation group. The total and differential cell counts in bronchoalveolar lavage fluid （BALF） were measured. TNF-α and IL-1β levels in BALF and serum were measured by ELISA. Malonaldehyde （MDA） level in lung tissue was detected by chromatometry. Emphysema changes were evaluated by mean linear intercept （MLI） of lung under light microscope by HE staining. Results The transfected MSC in different lung lobes were found to be alive at four weeks after intrapulmonary delivery. Compared with the emphysema group，the total cell count in BALF，TNF-α and IL-1β levels in BALF and serum，MDA level in lung tissue and MLI were significantly reduced intheMSCs transplantation group（Plt;0.01）. Conclusions Transplantation of MSCs can mediate down-regulation of TNF-α and IL-1β in BALF and serum，attenuate inflammation，oxidative stress and emphysema change of lung，suggesting that MSCs have significant therapeutic effects on emphysema.
循环纤维细胞是一类外周血中骨髓来源的间充质祖细胞, 其细胞表面表达造血细胞、单核细胞和成纤维细胞系的三种细胞标记, 参与组织应对损伤和破坏后的反应。根据近年来大量动物实验的研究, 循环纤维细胞的分化、迁移以及功能提示其在以慢性炎症和大量胶原沉积为特征的疾病中起着重要作用。尽管这些细胞参与疾病发生发展的具体机制仍然不清楚, 但是近年来积累的临床资料表明循环纤维细胞计数可以作为慢性肺部疾病( 包括肺纤维化、哮喘) 进展的生物学标志。通过免疫调节来影响循环纤维细胞的分化、迁移以及功能, 进而改善慢性炎症并减少胶原沉积, 可能成为治疗慢性肺部疾病特别是肺纤维化研究的新方向。
Objective To investigate and analyze the relationships among glucagon-like peptide-1 (GLP-1) level, chronic inflammation, and atherosclerosis in patients with non-alcoholic fatty liver disease (NAFLD). Methods From October 2016 to February 2017, using cross-sectional investigation, the GLP-1 level, chronic inflammation, and atherosclerosis were investigated in 80 subjects (40 NAFLD patients in NAFLD group, and 40 non-fatty liver disease participants in control group) who underwent physical examination at Xi’an Road Community Hospital. Results Compared with those in the control group, GLP-1 fasting level in patients with NAFLD [(9.09±1.03) vs. (9.15±1.06) pmol/L, P=0.807] and postprandial plasma GLP-1 [(15.96±3.37) vs. (17.46±4.76) pmol/L, P=0.108] had no changes. The correlations of GLP-1 level with chronic inflammation and insulin resistance (IR) were not significant either. The increased risk of carotid intima-media thickness related cardiovascular disease (CVD) in the NAFLD group was greater than that in the control group, and the difference was statistically significant [22 (55.0%)vs.13 (32.5%), P=0.043]. When the plasma lipoprotein-associated phospholipase A2 level increased, the risk of NAFLD increased [odd ratio (OR)=1.16, 95% confidence interval (CI) (1.02, 1.32), P=0.023]. Plasma ceramide kinase (CERK) in the NAFLD group was lower than that in the control group, and the difference was statistically significant [(12.36±2.45) vs. (18.33±3.71) ng/mL, P<0.001]. When the plasma CERK level of the fasting plasma was elevated, the risk of NAFLD decreased [OR=0.30, 95%CI (0.12, 0.78), P=0.014]. The homeostasis model assessment of insulin resistance (HOMA-IR) in the NAFLD group was higher than that in the control group, and the difference was statistically significant (2.46±2.53 vs. 1.11±0.66, P=0.002). The Matsuda index in the NAFLD group was less than that in the control group, and the difference was statistically significant (5.88±4.09 vs. 10.46±7.90, P=0.002). When HOMA-IR increased, the risk of NAFLD increased [OR=2.75, 95%CI (2.49, 3.12), P=0.036]. Conclusions Plasma GLP-1 level is not a sensitive indicator of chronic inflammation and IR in patients with NAFLD. Patients with NAFLD are in an increased risk of atherosclerosis and CVD. It suggests that NAFLD might be involved in chronic inflammation and IR. Chronic inflammation can cause IR, and then chronic inflammation and IR can cause NAFLD and subclinical atherosclerosis. In return for this, NAFLD increases chronic inflammation and IR.
Objective To summarize the research progress on the role of macrophage-mediated osteoimmune in osteonecrosis of the femoral head (ONFH) and its mechanisms. Methods Recent studies on the role and mechanism of macrophage-mediated osteoimmune in ONFH at home and abroad were extensively reviewed. The classification and function of macrophages were summarized, the osteoimmune regulation of macrophages on chronic inflammation in ONFH was summarized, and the pathophysiological mechanism of osteonecrosis was expounded from the perspective of osteoimmune, which provided new ideas for the treatment of ONFH. Results Macrophages are important immune cells involved in inflammatory response, which can differentiate into classically activated type (M1) and alternatively activated type (M2), and play specific functions to participate in and regulate the physiological and pathological processes of the body. Studies have shown that bone immune imbalance mediated by macrophages can cause local chronic inflammation and lead to the occurrence and development of ONFH. Therefore, regulating macrophage polarization is a potential ONFH treatment strategy. In chronic inflammatory microenvironment, inhibiting macrophage polarization to M1 can promote local inflammatory dissipation and effectively delay the progression of ONFH; regulating macrophage polarization to M2 can build a local osteoimmune microenvironment conducive to bone repair, which is helpful to necrotic tissue regeneration and repair to a certain extent. Conclusion At present, it has been confirmed that macrophage-mediated chronic inflammatory immune microenvironment is an important mechanism for the occurrence and development of ONFH. It is necessary to study the subtypes of immune cells in ONFH, the interaction between immune cells and macrophages, and the interaction between various immune cells and macrophages, which is beneficial to the development of potential therapeutic methods for ONFH.