旋毛虫重组53-kDa蛋白通过促进M2巨噬细胞极化减轻肺焦亡对小鼠急性肺损伤的保护作用。

IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Innate Immunity Pub Date : 2021-05-01 Epub Date: 2021-05-20 DOI:10.1177/17534259211013397
Ling-Yu Wei, An-Qi Jiang, Ren Jiang, Si-Ying Duan, Xue Xu, Ze-da-Zhong Su, Jia Xu
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引用次数: 8

摘要

旋毛虫是治疗自身免疫性疾病和炎症性疾病的有效方法。重组螺旋体(TS) 53-kDa蛋白(rTsP53)对急性肺损伤(ALI)的影响尚不清楚。将小鼠随机分为对照组、LPS组和rTsP53 + LPS组。通过尾静脉注射LPS (10 mg/kg)诱导BALB/c小鼠ALI。rTsP53(200µl;rTsP53+LPS组在诱导ALI前,每隔5 d皮下注射3次0.4 μg/ l。观察大鼠肺病理评分、经典活化巨噬细胞(M1)与交替活化巨噬细胞(M2)的比值及标志物、肺泡灌洗液细胞因子谱及肺组织焦亡蛋白表达。RTsP53降低肺病理评分。此外,rTsP53通过增加IL-4、IL-10和IL-13来抑制炎症。肺泡M2巨噬细胞数量增加,CD206和精氨酸酶-1阳性细胞增加,肺泡M1标记物如CD197和iNOS减少。此外,rTsP53诱导的M2巨噬细胞极化可以通过抑制肺焦亡来缓解ALI。RTsP53通过促进M2巨噬细胞极化减轻肺焦亡,被认为是治疗lps诱导ALI的潜在药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Protective effects of recombinant 53-kDa protein of <i>Trichinella spiralis</i> on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization.

Protective effects of recombinant 53-kDa protein of <i>Trichinella spiralis</i> on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization.

Protective effects of recombinant 53-kDa protein of <i>Trichinella spiralis</i> on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization.

Protective effects of recombinant 53-kDa protein of Trichinella spiralis on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization.

Trichinella spiralis represents an effective treatment for autoimmune and inflammatory diseases. The effects of recombinant T. spiralis (TS) 53-kDa protein (rTsP53) on acute lung injury (ALI) remain unclear. Here, mice were divided randomly into a control group, LPS group, and rTsP53 + LPS group. ALI was induced in BALB/c mice by LPS (10 mg/kg) injected via the tail vein. rTsP53 (200 µl; 0.4 μg/μl) was injected subcutaneously three times at an interval of 5 d before inducing ALI in the rTsP53+LPS group. Lung pathological score, the ratio and markers of classic activated macrophages (M1) and alternatively activated macrophages (M2), cytokine profiles in alveolar lavage fluid, and pyroptosis protein expression in lung tissue were investigated. RTsP53 decreased lung pathological score. Furthermore, rTsP53 suppressed inflammation by increasing IL-4, IL-10, and IL-13. There was an increase in alveolar M2 macrophage numbers, with an increase in CD206 and arginase-1-positive cells and a decrease in alveolar M1 markers such as CD197 and iNOS. In addition, the polarization of M2 macrophages induced by rTsP53 treatment could alleviate ALI by suppressing lung pyroptosis. RTsP53 was identified as a potential agent for treating LPS-induced ALI via alleviating lung pyroptosis by promoting M2 macrophage polarization.

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来源期刊
Innate Immunity
Innate Immunity 生物-免疫学
CiteScore
7.20
自引率
0.00%
发文量
20
审稿时长
6-12 weeks
期刊介绍: Innate Immunity is a highly ranked, peer-reviewed scholarly journal and is the official journal of the International Endotoxin & Innate Immunity Society (IEIIS). The journal welcomes manuscripts from researchers actively working on all aspects of innate immunity including biologically active bacterial, viral, fungal, parasitic, and plant components, as well as relevant cells, their receptors, signaling pathways, and induced mediators. The aim of the Journal is to provide a single, interdisciplinary forum for the dissemination of new information on innate immunity in humans, animals, and plants to researchers. The Journal creates a vehicle for the publication of articles encompassing all areas of research, basic, applied, and clinical. The subject areas of interest include, but are not limited to, research in biochemistry, biophysics, cell biology, chemistry, clinical medicine, immunology, infectious disease, microbiology, molecular biology, and pharmacology.
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