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感染在免疫抑制大鼠肺炎模型慢性阻塞性肺疾病进展中的作用。

Role of infection in chronic obstructive pulmonary disease progression in an immunosuppressed rat pneumonia model.

作者信息

Xue Ting, Chun-Li An

机构信息

Department of Microbiology and Parasitology, College of Basic Medical Science, China Medical University, Shenyang, Liaoning 110122, P.R. China.

出版信息

Exp Ther Med. 2020 Apr;19(4):3133-3142. doi: 10.3892/etm.2020.8545. Epub 2020 Feb 24.

DOI:10.3892/etm.2020.8545
PMID:32256801
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7086178/
Abstract

, an opportunistic fungal pathogen, is the primary cause of pneumonia (PCP), which affects immunocompromised individuals and leads to high morbidity and mortality. colonization is associated with development of chronic obstructive pulmonary disease (COPD) in patients with HIV infection, and also non-sufferers, and in primate models of HIV infection. However, the mechanisms underlying infection in the pathogenesis of COPD have yet to be fully elucidated. To investigate the pathogenicity of infection and its role in COPD development, the present study established a PCP rat model induced by dexamethasone sodium phosphate injection. Expression of COPD-related biomarkers, including matrix metalloproteinases (MMPs) MMP-2, MMP-8, MMP-9, and MMP-12, and heat shock protein-27 (HSP-27), were quantified in the rat PCP model using reverse transcription-quantitative polymerase chain reaction, ELISA, western blot analysis, immunohistochemistry and gelatin zymography. Body weight, COPD symptoms, and pulmonary histopathology were assessed. Inflammatory cell counts in splenic tissues were measured using flow cytometry. It was identified that MMP and HSP-27 expression increased in the PCP rats, which was in agreement with previous literature. Therefore, it was hypothesized that infection may have an important role in COPD development.

摘要

作为一种机会性真菌病原体,是肺孢子菌肺炎(PCP)的主要病因,该病影响免疫功能低下的个体并导致高发病率和死亡率。在HIV感染患者以及非HIV感染者和HIV感染的灵长类动物模型中,定植与慢性阻塞性肺疾病(COPD)的发生有关。然而,COPD发病机制中感染的潜在机制尚未完全阐明。为了研究感染的致病性及其在COPD发展中的作用,本研究建立了由地塞米松磷酸钠注射诱导的PCP大鼠模型。使用逆转录定量聚合酶链反应、酶联免疫吸附测定、蛋白质免疫印迹分析、免疫组织化学和明胶酶谱法,对大鼠PCP模型中与COPD相关的生物标志物的表达进行了定量,这些生物标志物包括基质金属蛋白酶(MMPs)MMP-2、MMP-8、MMP-9和MMP-12,以及热休克蛋白27(HSP-27)。评估了体重、COPD症状和肺组织病理学。使用流式细胞术测量脾组织中的炎性细胞计数。结果发现PCP大鼠中MMP和HSP-27表达增加,这与先前的文献一致。因此,推测感染可能在COPD发展中起重要作用。

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