This study explored the link between clinical features, immune markers, and asthma-chronic obstructive pulmonary disease overlap (ACO), aiming to enhance diagnostic precision and tailor treatment. The study included 60 patients per group: COPD patients, ACO patients, and healthy controls. Biological indicators such as fractional exhaled nitric oxide (FeNO), eosinophils, immunoglobulin E (IgE), T helper (Th) 17 cell counts, regulatory T-cell (Treg) counts, and cytokine levels of interleukin-17 (IL-17) and interleukin-10 (IL-10) were measured using standard enzyme-linked immunosorbent assay and flow cytometry techniques. Elevated Th17 cells, IL-17, and Th17/Treg ratio, alongside reduced IL-10 and Treg levels, were observed in COPD and ACO patients. ACO patients showed worse lung function, with a negative correlation between FeNO, Th17 cells, Th17/Treg ratio, IL-17, and lung function indices, and a positive correlation with residual volume/total lung capacity (RV/TLC) ratio. The study suggests that Th17/Treg imbalance, FeNO, eosinophils, and IgE could be key in ACO pathogenesis, potentially aiding early diagnosis and targeted treatment. Future research may utilize these findings to develop preventative and therapeutic strategies for ACO.

目的 探析铜绿假单胞菌介导线粒体DNA(mtDNA)/Toll样受体 9(TLR9)信号通路在支气管扩张症免疫失衡的作用机制.方法 选取 30 只雄性SPF级Wistar大鼠,10 只大鼠作为空白组,另外 20 只建立支气管扩张症模型,将建模成功的 20 只大鼠分为假手术组和模型组,各 10 只.空白组不做特殊处理;模型组注射 0.5 ml的铜绿假单胞菌液及 0.5 ml气体;假手术组注射 0.5 ml的生理盐水及 0.5 ml气体.采用苏木素-伊红(Hematoxylin-eosin,HE)染色对大鼠肺组织中支气管情况进行病理学观察,检测大鼠0.3 s用力呼吸容积(forced expiratory volume in 0.3 second,FEV0.3)、用力肺活量(forced vital capacity,FVC)、0.3 s用力呼吸容积/用力肺活量(forced expiratory volume in 0.3 second/forced vital capacity,FEV0.3/FVC)、用力呼气峰值流速(forced peak expiratory velocity,PEF)水平;酶联免疫吸附实验法检测高迁移率族蛋白B1(high mobility group box-B1,HMGB1)、干扰素-γ(Gamma interferon,IFN-γ)、白细胞介素-6(Interleukin-6,IL-6)、转化生长因子-β(transforming growth factor-β,TGF-β)水平;流式细胞仪检测辅助性T细胞 17(T helper cells 17,Th17)、调节性T细胞(T regulatory cell,Treg)、Th17/Treg细胞因子水平.结果 病理学分析中,空白组大鼠肺组织内支气管组织正常,假手术组大鼠支气管组织受到轻微损伤,模型组大鼠支气管组织出现严重损伤.与空白组相比,假手术组、模型组FEV0.3、FVC、PEF、IFN-γ、TGF-β、Treg水平降低(P＜0.05);FEV0.3/FVC、HMGB1、IL-6、Th17、Th17/Treg水平及mtDNA、TLR9 相对表达量均升高(P＜0.05).与假手术组相比,模型组Th17 水平升高,Treg水平降低,Th17/Treg水平升高,差异具有统计学意义(P＜0.05).结论 铜绿假单胞菌介导mtDNA/TLR9 信号通路在支气管扩张症中能够造成炎症反应升高,并且影响免疫功能,造成免疫失衡.

目的 重点分析慢阻肺合并重症呼吸衰竭患者接受无创呼吸机治疗后的临床效果。方法 在呼吸内科收治的慢阻肺合并重症呼吸衰竭患者中随机选择120例参与研究对象，以上患者均在2020年1月-2021年12月到院就诊，利用红蓝球抽签法分组，抽中红色球的60例合并症患者接受临床常规疗法作为对照组，另外60例合并症患者则接受无创呼吸机疗法归为观察组，比较以下指标：临床治疗效果、血气分析指标、生理指标、炎症因子水平、副作用发生率。结果 ①观察组总有效率与对照组总有效率明显更高，其值为95.0%、80.0%，两组临床效果差异存在统计学意义（P<0.05）；②治疗前，两组合并症患者的血气分析指标无明显差异（P>0.05）；治疗后，观察组SaO2、PaO2、PaCO2血气分析指标改善效果与对照组相比更加显著，两组血气分析指标差异有统计学意义（P<0.05）；③观察组呼吸频率、心率治疗期间稳定性与对照组相比明显更好，两组生命体征稳定性对比差异明显（P<0.05）；④观察组TNF-α、IL-8、IL-10等炎性因子水平改善效果与对照组改善效果相比明显更好，两组炎性因子水平对比有统计学意义（P<0.05）；⑤观察组副作用发生率为8.3%，对照组副作用发生率为21.7%，两组药物副作用发生率有统计学意义（P<0.05）。结论 慢阻肺合并重症呼吸衰竭患者接受无创呼吸机后，血气指标、生理指标和炎症因子水平均得到良好改善，总体临床治疗效果明显升高，且治疗后副作用发生率较低，这种方法的有效性与安全性显著，是一项值得积极推广的应用。

目的 探讨铜绿假单胞菌感染对支气管扩张发病的作用机制,为该病的临床治疗提供理论依据.方法 将30只SD大鼠按随机数字表法分为正常对照组、假手术组和支气管扩张模型组(模型组),每组10只,对大鼠气管注射铜绿假单胞菌,把支气管扩张模型建立起来;假手术组只做气管切开后缝合,正常对照组不予任何处理.术后第14天测定3组大鼠一般情况,苏木素-伊红(HE)染色观察肺组织病理学改变,流式细胞术测定外周血辅助性T细胞17(T helper cell 17,Th17)和调节性T细胞(T regulatory cell,Treg)的表达,酶联免疫吸附试验(ELISA)检测血清白细胞介素(IL)-17、IL-6、IL-10、转化生长因子(TGF)-β的表达.结果 与正常对照组和假手术组比较,模型组用力肺活量(FVC)、0.3 s用力呼吸容积(FEV0.3)、用力呼气峰值流速(PEF)明显下降,而FEV0.3/FVC比值升高(P<0.05).光镜下观察,模型组大鼠支气管扩张明显,有明显的炎症病理性改变.模型组与正常对照组、假手术组分别比较,血清IL-17明显升高(P<0.01)、IL-6明显升高(P<0.01)、IL-10明显降低(P<0.01)、TGF-β明显降低(P<0.01)、Th17表达显著升高(P<0.01)、Treg表达明显降低(P<0.01)、Th17/Treg比值升高(P<0.01).结论 铜绿假单胞菌介导的支气管扩张大鼠炎症反应升高,与Th17/Treg表达失衡有关,导致肺功能下降.

目的 研究乙酰半胱氨酸雾化吸入对支气管扩张症患者的临床治疗效果.方法 75例支气管扩张症患者,随机分为对照组(37例)和观察组(38例).对照组采用生理盐水雾化吸入治疗,观察组采用乙酰半胱氨酸雾化吸入治疗.比较两组患者的疗效,肺功能指标[第1秒用力呼气容积(FEV1)、用力肺活量(FVC)、呼气峰值流速(PEF)],咳痰量、咳嗽次数评分,生活质量评分.结果 观察组总有效率为92.11％(35/38),高于对照组的72.97％(27/37),差异具有统计学意义(P<0.05).观察组患者的FEV1、FVC、PEF均高于对照组,差异均具有统计学意义(P<0.05).观察组患者的咳痰量评分(1.62±0.73)分、咳嗽次数评分(1.20±0.63)分均低于对照组的(2.71±0.98)、(1.57±0.86)分,差异均具有统计学意义(P<0.05).观察组患者的生活质量评分(33.49±5.37)分低于对照组的(40.53±6.54)分,差异具有统计学意义(P<0.05).结论 乙酰半胱氨酸雾化吸入对支气管扩张症患者的治疗效果较好,明显地改善了患者的肺功能,减少咳痰量和咳嗽次数,提高患者的生活质量.

BACKGROUND The prevalence of bronchiectasis with comorbid chronic obstructive pulmonary disease (COPD) is rising, which causes extremely high risk of exacerbation and mortality. We aimed to evaluate the differences in clinicopathological manifestations, immune function, and inflammation in bronchiectasis patients with comorbid COPD vs. patients who only have COPD. MATERIAL AND METHODS Clinicopathological characteristics, including common potentially pathogenic microorganisms, lung function, immune function, and inflammation were assessed in bronchiectasis patients with comorbid COPD and in patients who only had COPD. RESULTS Compared to patients who only had COPD, patients with bronchiectasis with comorbid COPD had a higher positive rate of sputum bacteria (45.27% vs. 28.03%, P<0.01). Among them, Pseudomonas aeruginosa (P. aeruginosa) accounted for 25.19% in COPD (4.37%) (P<0.01). Likewise, patients with bronchiectasis with comorbid COPD had worse lung function, worse COPD assessment test scores, and worse Modified Medical Research Council scores. Moreover, compared with COPD only cases, patients with bronchiectasis with comorbid COPD had higher levels of white blood cells (WBC), neutrophils, C-reactive protein (CRP), and procalcitonin (PCT) (all P<0.05). Interestingly, the expression levels of Treg in patients with bronchiectasis with comorbid COPD were lower than in patients with COPD only (P<0.05). Th17 and Th17/Treg levels were higher (P<0.05). Furthermore, remarkable increased level of IL17 and IL-6 and decreased level of IL-10 and TGF-ß were observed in the bronchiectasis combined COPD than in pure COPD (All P<0.05). CONCLUSIONS Our findings suggest that P. aeruginosa is the main pathogen of bacterial infection in bronchiectasis patients with comorbid COPD. These patients have more serious clinical manifestations and immune imbalance, which should be considered when providing clinical treatment.