Open AccessProtective effects of recombinant 53-kDa protein of Trichinella spiralis on acute lung injury in mice via alleviating lung pyroptosis by promoting M2 macrophage polarization
Author(s) -
Lingyu Wei,
An-qi Jiang,
Jing Ren,
Si-ying Duan,
Xiaonan Xue,
Zedazhong Su,
Jiacheng Xu
Publication year - 2021
Publication title -
innate immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.921
H-Index - 69
eISSN - 1753-4267
pISSN - 1753-4259
DOI - 10.1177/17534259211013397
Subject(s) - pyroptosis , trichinella spiralis , lung , macrophage polarization , inflammation , immunology , alveolar macrophage , medicine , m2 macrophage , proinflammatory cytokine , macrophage , chemistry , inflammasome , antigen , in vitro , biochemistry
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.