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嗜铁素 Lcn2 通过调控巨噬细胞功能缓解 LPS 引起的炎症
Authors Du H, Liang L, Li J, Xiong Q, Yu X, Yu H
Received 11 July 2021
Accepted for publication 13 August 2021
Published 26 August 2021 Volume 2021:14 Pages 4189—4203
DOI https://doi.org/10.2147/JIR.S328916
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Ning Quan
摘要：① LPS 刺激能显著上调嗜铁素 Lcn2 在小鼠肝脏、空肠、回肠等组织中的表达。② 敲除 Lcn2 可使 LPS 刺激小鼠的炎症症状加剧，肠道绒毛受损，促炎因子分泌增加。③ LPS 刺激后，Lcn2 在肝脏巨噬细胞中高表达，亚细胞定位发现其主要在巨噬细胞的胞质中表达。④ 敲除 Lcn2 能加剧巨噬细胞的炎症应答，促炎因子显著上调，抑炎因子显著下调，而添加 Lcn2 则能逆转其反应。⑤ 敲除 Lcn2 小鼠的巨噬细胞显著上调炎症相关通路蛋白，但其吞噬和自噬功能下降。以上结果说明 Lcn2 是系统性炎症应激的保护因子，也是炎症过程中巨噬细胞发挥其功能不可或缺的细胞因子。
Keywords: Lcn2, systemic inflammation, macrophages, BMDMs