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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
Innate Immunity ( IF 3.2 ) Pub Date : 2021-05-20 , DOI: 10.1177/17534259211013397
Ling-Yu Wei 1 , An-Qi Jiang 1 , Ren Jiang 1 , Si-Ying Duan 1 , Xue Xu 1 , Ze-da-Zhong Su 2 , Jia Xu 1
Affiliation  

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.



中文翻译:

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

旋毛虫代表了对自身免疫和炎症性疾病的有效治疗。重组T.spiralis的作用(TS) 53-kDa 蛋白 (rTsP53) 对急性肺损伤 (ALI) 的影响仍不清楚。在这里,将小鼠随机分为对照组、LPS组和rTsP53 + LPS组。通过尾静脉注射的 LPS (10 mg/kg) 在 BALB/c 小鼠中诱导 ALI。在 rTsP53+LPS 组诱导 ALI 前,每隔 5 天皮下注射 3 次 rTsP53(200 μl;0.4 μg/μl)。研究了肺病理学评分、经典活化巨噬细胞 (M1) 和交替活化巨噬细胞 (M2) 的比例和标志物、肺泡灌洗液中的细胞因子谱以及肺组织中焦亡蛋白的表达。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 标志物如 CD197 和 iNOS 减少。此外,rTsP53 诱导的 M2 巨噬细胞极化可通过抑制肺焦亡来缓解 ALI。RTsP53 被确定为通过促进 M2 巨噬细胞极化减轻肺焦亡来治疗 LPS 诱导的 ALI 的潜在药物。

更新日期:2021-05-20
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