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鉴定通过中性粒细胞胞外诱捕网吞噬作用产生促甲状腺激素释放激素的巨噬细胞的来源器官。

Identification of organs of origin of macrophages that produce presepsin via neutrophil extracellular trap phagocytosis.

机构信息

Laboratory of Hematology, Department of Medical Technology, Kagawa Prefectural University of Health Sciences, 281-1, Hara, Mure-cho, Takamatsu, Kagawa, 761-0123, Japan.

Laboratory of Pathology, Department of Medical Technology, Kagawa Prefectural University of Health Sciences, Takamatsu, Kagawa, Japan.

出版信息

Sci Rep. 2024 Jul 16;14(1):16386. doi: 10.1038/s41598-024-66916-y.

Abstract

Presepsin (P-SEP) is a specific biomarker for sepsis. Monocytes produce P-SEP by phagocytosing neutrophil extracellular traps (NETs). Herein, we investigated whether M1 macrophages (M1 MΦs) are the primary producers of P-SEP after NET phagocytosis. We co-cultured M1 MΦs and NETs from healthy participants, measured P-SEP levels in the culture medium supernatant, and detected P-SEP using western blotting. When NETs were co-cultured with M1 MΦs, the P-SEP level of the culture supernatant was high. Notably, we demonstrated, for the first time, the intracellular kinetics of P-SEP production by M1 MΦs via NET phagocytosis: M1 MΦs produced P-SEP intracellularly 15 min after NET phagocytosis and then released it extracellularly. In a sepsis mouse model, the blood NET ratio and P-SEP levels, detected using ELISA, were significantly increased (p < 0.0001). Intracellular P-SEP analysis via flow cytometry demonstrated that lung, liver, and kidney MΦs produced large amounts of P-SEP. Therefore, we identified these organs as the origin of M1 MΦs that produce P-SEP during sepsis. Our data indicate that the P-SEP level reflects the trend of NETs, suggesting that monitoring P-SEP can be used to both assess NET-induced organ damage in the lungs, liver, and kidneys during sepsis and determine treatment efficacy.

摘要

促炎因子(P-SEP)是脓毒症的特异性生物标志物。单核细胞通过吞噬中性粒细胞细胞外陷阱(NETs)产生 P-SEP。在此,我们研究了在吞噬 NET 后,M1 巨噬细胞(M1 MΦs)是否是 P-SEP 的主要产生者。我们共培养了来自健康参与者的 M1 MΦs 和 NETs,测量了培养基上清液中的 P-SEP 水平,并使用 Western blot 检测了 P-SEP。当 NETs 与 M1 MΦs 共培养时,培养基上清液中的 P-SEP 水平较高。值得注意的是,我们首次通过 NET 吞噬作用证明了 M1 MΦs 产生 P-SEP 的细胞内动力学:M1 MΦs 在吞噬 NET 后 15 分钟内在细胞内产生 P-SEP,然后将其释放到细胞外。在脓毒症小鼠模型中,通过 ELISA 检测到血液 NET 比例和 P-SEP 水平显著增加(p<0.0001)。通过流式细胞术进行的细胞内 P-SEP 分析表明,肺、肝和肾 MΦs 产生大量 P-SEP。因此,我们将这些器官确定为脓毒症期间产生 P-SEP 的 M1 MΦs 的来源。我们的数据表明,P-SEP 水平反映了 NETs 的趋势,提示监测 P-SEP 可用于评估脓毒症期间肺部、肝脏和肾脏中 NET 诱导的器官损伤,并确定治疗效果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f8f9/11252129/62a2909b7790/41598_2024_66916_Fig1_HTML.jpg

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