自发性脑出血患者肺部感染相关炎症因子与TLR4/NF-κB信号通路的相互作用

IF 3.7 3区 医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Cytokine Pub Date : 2025-02-01 Epub Date: 2025-01-03 DOI:10.1016/j.cyto.2024.156851
Bo Tan, Tao Chen, Peng Song, Feng Lin, Shuangyin He, Shiyuan Zhang, Xiaohong Yin
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引用次数: 0

摘要

目的:探讨自发性脑出血(ICH)患者肺部感染相关炎症因子与TLR4/NF-κB信号通路的相互作用。方法:选择我院2021年5月至2024年2月收治的脑出血危重症患者325例。根据患者在治疗过程中是否发生肺部感染分为感染组(n = 86)和非感染组(n = 239)。观察病原菌分布特点,比较血清及防御素、hs-CRP、IL-4、TLR4 mRNA、NF-κB mRNA的变化。采用Pearson相关分析分析血清防御素、炎症因子与TLR4/NF-κB信号通路的关系。采用logistic回归模型构建防御素、hs-CRP、IL-4、HMGB1、TLR4 mRNA、NF-κB mRNA联合预测模型。绘制ROC曲线,分析防御素、hs-CRP、IL-4、HMGB1、TLR4 mRNA、NF-κB mRNA及6项综合参数预测脑出血危重症患者肺部感染的曲线下面积(AUC)、敏感性和特异性。结果:86例脑出血肺部感染患者共分离病原菌94株,其中革兰氏阳性菌28株(29.79%),革兰氏阴性菌58株(61.70%),真菌8株(8.51%)。感染组患者的防御素、hs-CRP、IL-4、HMGB1、TLR4 mRNA、NF-κB mRNA水平均显著高于非感染组(P)。结论:致重症脑出血患者肺部感染的主要病原体为肺炎克雷伯菌、铜绿假单胞菌、鲍曼不动杆菌、金黄色葡萄球菌、溶血性链球菌。继发性肺部感染患者的防御素、hs-CRP、IL-4、HMGB1等指标受TLR4/NF-κB信号通路的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Interaction of inflammatory factors related to pulmonary infection and TLR4/NF-κB signaling pathway in patients with spontaneous intracerebral hemorrhage.

Objective: To investigate the interaction of inflammatory factors related to pulmonary infection and the TLR4/NF-κB signaling pathway in patients with spontaneous intracerebral hemorrhage (ICH).

Methods: A total of 325 critically ill ICH patients treated in our hospital from May 2021 to February 2024 were selected for this study. Based on whether the patient developed a pulmonary infection during treatment, they were divided into the infection group (n = 86) and the non-infection group (n = 239). The distribution characteristics of pathogens were observed, and changes in serum and defensin, hs-CRP, IL-4, TLR4 mRNA, and NF-κB mRNA were compared. Pearson correlation analysis was used to analyze the relationship between serum defensin, inflammatory factors, and the TLR4/NF-κB signaling pathway. A logistic regression model was used to construct a combined prediction model with defensin, hs-CRP, IL-4, HMGB1, TLR4 mRNA, and NF-κB mRNA. ROC curves were drawn to analyze the area under the curve (AUC), sensitivity, and specificity of defensin, hs-CRP, IL-4, HMGB1, TLR4 mRNA, NF-κB mRNA, and the six combined parameters for predicting pulmonary infection in critically ill ICH patients.

Results: In 86 ICH patients with pulmonary infection, 94 strains of pathogens were isolated, with 28 (29.79 %) Gram-positive bacteria, 58 (61.70 %) Gram-negative bacteria, and 8 (8.51 %) fungi. The levels of defensin, hs-CRP, IL-4, HMGB1, TLR4 mRNA, and NF-κB mRNA in the infection group were significantly higher than those in the non-infection group (P < 0.05). Pearson correlation analysis showed that defensin, hs-CRP, IL-4, and HMGB1 were positively correlated with TLR4 mRNA and NF-κB mRNA (P < 0.05). ROC curve analysis showed that the AUC values for defensin, hs-CRP, IL-4, HMGB1, TLR4 mRNA, NF-κB mRNA, and the six combined parameters for predicting pulmonary infection were 0.789, 0.778, 0.690, 0.792, 0.741, 0.750, and 0.870, respectively.

Conclusion: The main pathogens causing pulmonary infection in critically ill ICH patients are Klebsiella pneumoniae, Pseudomonas aeruginosa, Acinetobacter baumannii, Staphylococcus aureus, and Streptococcus hemolyticus. Defensin, hs-CRP, IL-4, HMGB1, and other indicators are influenced by the TLR4/NF-κB signaling pathway in patients with secondary pulmonary infection.

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来源期刊
Cytokine
Cytokine 医学-免疫学
CiteScore
7.60
自引率
2.60%
发文量
262
审稿时长
48 days
期刊介绍: The journal Cytokine has an open access mirror journal Cytokine: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. * Devoted exclusively to the study of the molecular biology, genetics, biochemistry, immunology, genome-wide association studies, pathobiology, diagnostic and clinical applications of all known interleukins, hematopoietic factors, growth factors, cytotoxins, interferons, new cytokines, and chemokines, Cytokine provides comprehensive coverage of cytokines and their mechanisms of actions, 12 times a year by publishing original high quality refereed scientific papers from prominent investigators in both the academic and industrial sectors. We will publish 3 major types of manuscripts: 1) Original manuscripts describing research results. 2) Basic and clinical reviews describing cytokine actions and regulation. 3) Short commentaries/perspectives on recently published aspects of cytokines, pathogenesis and clinical results.
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