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巨噬细胞凋亡抑制剂改善小鼠真菌性腹膜炎损伤模型。

Apoptosis inhibitor of macrophage ameliorates fungus-induced peritoneal injury model in mice.

机构信息

Department of Nephrology and Renal Replacement Therapy, Nagoya University Graduate School of Medicine, Nagoya, Japan.

Laboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, University of Tokyo, Tokyo, Japan.

出版信息

Sci Rep. 2017 Jul 25;7(1):6450. doi: 10.1038/s41598-017-06824-6.

DOI:10.1038/s41598-017-06824-6
PMID:28743989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5527077/
Abstract

Fungal peritonitis in a patient on peritoneal dialysis (PD) is a refractory injury accompanied by severe inflammation, predisposing patients to a poor prognosis. Defective clearance of necrotic tissue interferes with amelioration of tissue injury and induces abnormal tissue remodeling. In the recent reports, apoptosis inhibitor of macrophage (AIM, also called CD5L) prevents obesity, hepatocellular carcinoma and acute kidney injury. Here, we investigated potential roles of AIM in prevention of progression of fungal peritonitis models. AIM mice subjected to zymosan-induced peritonitis exhibited progressive inflammation and sustained peritoneal necrosis tissue on day 28 after the disease induction, whereas there was an improvement in AIM mice. This appeared to be caused by deposition of AIM at the necrotic peritoneum in AIM mice. In vitro, AIM enhanced the engulfment of necrotic debris by macrophages derived from zymosan-induced peritonitis, M1- and M2a-like bone marrow derived macrophages, as well as by mesothelial cells. In addition, administration of recombinant AIM dramatically ameliorated severe inflammation associated with necrosis in zymosan-induced peritonitis of AIM mice. Our observations suggest that AIM appears to be involved in the repair process of zymosan-induced peritonitis, and thus, could be the basis of development of new therapeutic strategies for PD-related fungal peritonitis.

摘要

患者在腹膜透析（PD）中发生真菌性腹膜炎是一种难治性损伤，伴有严重炎症，使患者预后不良。坏死组织清除功能缺陷会干扰组织损伤的改善，并诱导异常组织重塑。在最近的报告中，巨噬细胞凋亡抑制剂（AIM，也称为 CD5L）可预防肥胖、肝细胞癌和急性肾损伤。在这里，我们研究了 AIM 在预防真菌性腹膜炎模型进展中的潜在作用。诱导产生 AIM 的小鼠在酵母聚糖诱导的腹膜炎后 28 天表现出进行性炎症和持续的腹膜坏死组织，而 AIM 小鼠则有所改善。这似乎是由于 AIM 在 AIM 小鼠的坏死腹膜中沉积所致。在体外，AIM 增强了源自酵母聚糖诱导的腹膜炎、M1 和 M2a 样骨髓来源巨噬细胞以及间皮细胞吞噬坏死碎片的能力。此外，重组 AIM 的给药可显著改善诱导产生 AIM 的小鼠的酵母聚糖诱导腹膜炎中与坏死相关的严重炎症。我们的观察结果表明，AIM 似乎参与了酵母聚糖诱导的腹膜炎的修复过程，因此，可能为 PD 相关真菌性腹膜炎的新治疗策略的发展提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5208/5527077/39030e239f8a/41598_2017_6824_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5208/5527077/58ff932c8618/41598_2017_6824_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5208/5527077/39030e239f8a/41598_2017_6824_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5208/5527077/58ff932c8618/41598_2017_6824_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5208/5527077/ba3e349d356e/41598_2017_6824_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5208/5527077/d18e27ecffe2/41598_2017_6824_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5208/5527077/e2b552d0cc82/41598_2017_6824_Fig4_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5208/5527077/39030e239f8a/41598_2017_6824_Fig7_HTML.jpg

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