IL-33 Enhances the Lipopolysaccharide-Induced Secretion of Inflammatory Cytokines and Ameliorates Lipopolysaccharide Desensitization in Macrophages
IL-33 Enhances the Lipopolysaccharide-Induced Secretion of Inflammatory Cytokines and Ameliorates Lipopolysaccharide Desensitization in Macrophages
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IL-33 增强脂多糖诱导的炎症细胞因子的分泌并改善巨噬细胞中的脂多糖脱敏
DOI：
10.1166/jbt.2022.2913
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发表时间：
2022-02
影响因子：
0.1
通讯作者：
Jing-Yan
中科院分区：
文献类型：
--
作者：
Dong-Yang Guo;Zhou-Xin Yang;Guo-Long Cai;Ling-Zhi Shen;Ying-Xing Yue;Jing-Yan
背景资料：脂多糖（LPS）脱敏，其特征在于低反应性和一种形式的免疫抑制，是重要的负性调节反应的LPS和炎症性疾病，如败血症。然而，IL-33在脱敏中的作用
LPS仍不清楚。方法：应用RNA测序技术分析LPS刺激骨髓源性巨噬细胞（BMDM）后mRNA的变化。分别用qPCR和ELISA检测炎性细胞因子表达和分泌的变化。机制是
通过p65磷酸化检测进一步研究。结果：LPS处理的巨噬细胞中IL-33表达显著增加，表明其参与LPS诱导的炎症。外源性IL-33可增加炎症反应，并改善LPS脱敏，
增加促炎细胞因子的分泌。它还激活了耐药细胞中的p65磷酸化。结论：IL-33可能通过激活NF-κB通路，增强LPS诱导的炎症反应，减轻LPS脱敏。
Background: Lipopolysaccharide (LPS) desensitization, which is characterized by hyporesponsiveness and a form of immunosuppression, is important in the negative regulation of responses to LPS and inflammatory disease such as sepsis. However, effect of IL-33 in the desensitization
to LPS remains unclear. Methods: We used RNA-sequencing technology to analyze changes in mRNA in bone-marrow-derived macrophages (BMDMs) stimulated with LPS. Changes in expression and secretion of inflammatory cytokines were detected by qPCR and ELISA, respectively. Mechanisms were
further studied through p65 phosphorylation detection. Results: IL-33 expression was significantly increased in LPS-treated macrophages, indicating its involvement in LPS-induced inflammation. Exogenous IL-33 increased the inflammatory response and ameliorated LPS desensitization by
increasing the secretion of proinflammatory cytokines. It also activated p65 phosphorylation in resistant cells. Conclusion: IL-33 can enhance the inflammatory response induced by LPS and ameliorate LPS desensitization possibly by activating the NF-κB pathway in mouse macrophages.