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慢性阻塞性肺疾病合并肺部感染患者的细菌谱、激活素A及CD64分析

Analysis of bacterial spectrum, activin A, and CD64 in chronic obstructive pulmonary disease patients complicated with pulmonary infections.

作者信息

Fei Zhao-Yang, Wang Jiang, Liang Jie, Zhou Xue, Guo Min

机构信息

Experimental Research Centre, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.

Department of Laboratory Medicine, Lianyungang Second People's Hospital, Lianyungang 222006, Jiangsu Province, China.

出版信息

World J Clin Cases. 2022 Mar 16;10(8):2382-2392. doi: 10.12998/wjcc.v10.i8.2382.

DOI:10.12998/wjcc.v10.i8.2382
PMID:35434072
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8968607/
Abstract

BACKGROUND

Pulmonary infections often lead to poor prognoses in patients with chronic obstructive pulmonary disease (COPD). Activin A and CD64 play crucial pathological roles in the development of COPD.

AIM

To explore the bacterial spectrum analysis of activing A levels, CD64 index, and related mechanisms in COPD patients complicated with pulmonary infection.

METHODS

Between March 2015 and January 2018, a total of 85 patients with COPD, who also suffered from pulmonary infections, were enrolled in this study as the pulmonary infection group. In addition, a total of 96 COPD patients, without pulmonary infection, were selected as the control group. Sputum samples of patients in the pulmonary infection group were cultivated for bacterial identification prior to administration of antibiotics. The neutrophil CD64 index was measured using flow cytometry, serum activin A levels were detected an enzyme-linked immunosorbent assay, and activin A, Smad3, TLR4, MyD88, and NFκB protein expression was analyzed by Western blotting.

RESULTS

Gram-negative bacteria were identified in 57.65% of the sputum samples in the pulmonary infection group. The most prevalent Gram-negative species were and . Conversely, Gram-positive bacteria were identified in 41.18% of the sputum samples in the pulmonary infection group. The most common Gram-positive species was . Fungi were identified in 1.17% of the sputum samples in the pulmonary infection group. The CD64 index was significantly higher in the pulmonary infection group (0.91 ± 0.38) than in the control group (0.23 ± 0.14, < 0.001). The serum activin A levels were significantly higher in the pulmonary infection group (43.50 ± 5.22 ng/mL), compared to the control group (34.82 ± 4.16 ng/mL, < 0.001). The relative expression levels of activin A, Smad3, TLR4, MyD88, and NFκB were all significantly higher in the pulmonary infection group, compared to the control group (all < 0.001).

CONCLUSION

Pulmonary infections in COPD patients are mainly caused by , , and . Pulmonary infections can significantly increase neutrophil CD64 index and serum levels of activin A, thereby activating the activin A/Smad3 signaling pathway, which may positively regulate the TLR4/MyD88/NFκB signaling pathway.

摘要

背景

肺部感染常导致慢性阻塞性肺疾病(COPD)患者预后不良。激活素A和CD64在COPD的发展过程中发挥着关键的病理作用。

目的

探讨COPD合并肺部感染患者的细菌谱分析、激活素A水平、CD64指数及相关机制。

方法

2015年3月至2018年1月,本研究共纳入85例患有肺部感染的COPD患者作为肺部感染组。此外,选取96例无肺部感染的COPD患者作为对照组。肺部感染组患者在使用抗生素前采集痰液样本进行细菌鉴定。采用流式细胞术检测中性粒细胞CD64指数,酶联免疫吸附测定法检测血清激活素A水平,蛋白质免疫印迹法分析激活素A、Smad3、TLR4、MyD88和NFκB蛋白表达。

结果

肺部感染组57.65%的痰液样本中鉴定出革兰氏阴性菌。最常见的革兰氏阴性菌是[具体细菌名称1]和[具体细菌名称2]。相反,肺部感染组41.18%的痰液样本中鉴定出革兰氏阳性菌。最常见的革兰氏阳性菌是[具体细菌名称3]。肺部感染组1.17%的痰液样本中鉴定出真菌。肺部感染组的CD64指数(0.91±0.38)显著高于对照组(0.23±0.14,P<0.001)。肺部感染组的血清激活素A水平(43.50±5.22 ng/mL)显著高于对照组(34.82±4.16 ng/mL,P<0.001)。与对照组相比,肺部感染组激活素A、Smad3、TLR4、MyD88和NFκB的相对表达水平均显著升高(均P<0.001)。

结论

COPD患者的肺部感染主要由[具体细菌名称1]、[具体细菌名称2]和[具体细菌名称3]引起。肺部感染可显著增加中性粒细胞CD64指数和血清激活素A水平,从而激活激活素A/Smad3信号通路,这可能正向调节TLR4/MyD88/NFκB信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dced/8968607/172bf1bf182d/WJCC-10-2382-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dced/8968607/00122e60c8aa/WJCC-10-2382-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dced/8968607/b37079f065d5/WJCC-10-2382-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dced/8968607/172bf1bf182d/WJCC-10-2382-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dced/8968607/00122e60c8aa/WJCC-10-2382-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dced/8968607/b37079f065d5/WJCC-10-2382-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dced/8968607/172bf1bf182d/WJCC-10-2382-g003.jpg

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