Trichinella spiralis excretory/secretory products from adult worms inhibit NETosis and regulate the production of cytokines from neutrophils

文献类型： 外文期刊

第一作者： Wang, Jing

作者： Wang, Jing;Tang, Bin;Liu, Xiaolei;Liu, Mingyuan;Jin, Xuemin;Ding, Jing;Wang, Jing;Tang, Bin;Liu, Xiaolei;Liu, Mingyuan;Jin, Xuemin;Ding, Jing;You, Xihuo;Cai, Xuepeng;Jia, Wanzhong

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关键词： Trichinella spiralis; Excretory and secretory products; Neutrophil extracellular traps; Immune response

期刊名称：PARASITES & VECTORS （ 影响因子：3.2； 五年影响因子：3.6 ）

ISSN： 1756-3305

年卷期： 2023 年 16 卷 1 期

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收录情况： SCI

摘要： Upon encountering exogenous pathogens, polymorphonucleocytes (PMNs) engage in various processes to destroy them, including releasing neutrophil extracellular traps (NETs) that trap pathogens and induce phagocytosis and cytokine production. Parasites have unique strategies with which to evade the host's immune response. However, the strategy employed by Trichinella spiralis in response to the reaction of PMNs has yet to be elucidated. This study explored the effect of excretory/secretory products (ESP) on three major functions: NETs, phagocytosis, and cytokine production. Specifically, PMNs were pre-treated with the ESP of 3-day-old adults and then stimulated with phorbol 12-myristate 13-acetate (PMA). We found that in PMNs pretreated with ESP, PMA-induced NET generation was suppressed by ESP. ROS production is a hallmark of PMA-induced NETosis. The LDH assay results showed that ESP inhibits NETs by suppressing ROS rather than promoting PMN death. Furthermore, ESP enhanced Escherichia coli engulfment by PMNs, improving overall phagocytic function. Finally, cytokine analysis revealed an increase in pro-inflammatory cytokine IL-1 beta, and other cytokines (IL-10, TNF-alpha), while IL-4 displayed a significant reduction. In conclusion, this study has unraveled T. spiralis' evasion and regulation mechanisms against innate immune cells, providing insights into parasite strategies to manipulate host immunity, potentially informing new treatments for NET-related autoimmune diseases.

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