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Novel Sca-1+ macrophages modulate the pathogenic progress of endotoxemia.
Biochemical and Biophysical Research Communications ( IF 3.1 ) Pub Date : 2020-09-10 , DOI: 10.1016/j.bbrc.2020.08.118
Min Young Park 1 , Hyung Sik Kim 1 , Yu Sun Jeong 1 , Hye Young Kim 2 , Yoe-Sik Bae 1
Affiliation  

Macrophages are important innate immune cells that play crucial roles in inflammatory responses. Accumulating evidence has demonstrated macrophage heterogeneity based on biomarkers, functions, and localization. Here, we report a novel stem cell antigen-1 (Sca-1)-positive macrophage population induced in the pathological conditions caused by lipopolysaccharide (LPS). Sca-1 is only upregulated in macrophages but not in monocytes and neutrophils upon LPS injection. Sca-1+ macrophages develop from resident peritoneal macrophages. LPS-induced Sca-1+ macrophage generation was partly blocked by anti–IFN–γ antibody, suggesting a role of IFN-γ in the process. LPS-stimulated production of IL-6, TNF-α, and CCL2 is significantly lower in Sca-1+ macrophages compared to their counterpart Sca-1- macrophages. Depletion of Sca-1+ macrophages using anti-Sca-1 antibody significantly increased survival rate and reduced lung and kidney damage in an LPS-induced sepsis model. Taken together, we discovered a novel population of Sca-1+ macrophages in LPS-induced septic conditions.



中文翻译:

新型Sca-1 +巨噬细胞调节内毒素血症的致病过程。

巨噬细胞是重要的先天免疫细胞,在炎症反应中起关键作用。越来越多的证据表明,基于生物标记,功能和定位的巨噬细胞异质性。在这里,我们报告了一种新的干细胞抗原-1(Sca-1)阳性巨噬细胞群体在脂多糖(LPS)引起的病理条件下诱导。LPS注射后,Sca-1仅在巨噬细胞中上调,而在单核细胞和中性粒细胞中则不上调。Sca-1 +巨噬细胞从驻留的腹膜巨噬细胞发育而来。LPS诱导的Sca-1 +巨噬细胞的生成被抗IFN-γ抗体部分阻止,表明IFN-γ在该过程中发挥了作用。Lca刺激的Sca-1 +中IL-6,TNF-α和CCL2的产生明显降低巨噬细胞相比,其对应的Sca-1 -巨噬细胞。在LPS诱导的败血症模型中,使用抗Sca-1抗体消耗Sca-1 +巨噬细胞可显着提高生存率并减少肺和肾脏的损害。综上所述,我们在LPS诱导的败血症条件下发现了新的Sca-1 +巨噬细胞种群。

更新日期:2020-10-17
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