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实验性炎症性肠病小鼠巨噬细胞 PPAR-γ 的免疫调节机制。

Immunoregulatory mechanisms of macrophage PPAR-γ in mice with experimental inflammatory bowel disease.

机构信息

CyberInfrastructure Division, Virginia Bioinformatics Institute, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA.

出版信息

Mucosal Immunol. 2011 May;4(3):304-13. doi: 10.1038/mi.2010.75. Epub 2010 Nov 10.

DOI:10.1038/mi.2010.75
PMID:21068720
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3049196/
Abstract

Peroxisome proliferator-activated receptor-γ (PPAR-γ) is widely expressed in macrophages and has been identified as a putative target for the development of novel therapies against inflammatory bowel disease (IBD). Computational simulations identified macrophages as key targets for therapeutic interventions against IBD. This study aimed to characterize the mechanisms underlying the beneficial effects of macrophage PPAR-γ in IBD. Macrophage-specific PPAR-γ deletion significantly exacerbated clinical activity and colonic pathology, impaired the splenic and mesenteric lymph node regulatory T-cell compartment, increased percentages of lamina propria (LP) CD8+ T cells, increased surface expression of CD40, Ly6C, and Toll-like receptor 4 (TLR-4) in LP macrophages, and upregulated expression of colonic IFN-γ, CXCL9, CXCL10, IL-22, IL1RL1, CCR1, suppressor of cytokine signaling 3, and MHC class II in mice with IBD. Moreover, macrophage PPAR-γ was required for accelerating pioglitazone-mediated recovery from dextran sodium sulfate (DSS) colitis, providing a cellular target for the anti-inflammatory effects of PPAR-γ agonists in IBD.

摘要

过氧化物酶体增殖物激活受体-γ（PPAR-γ）在巨噬细胞中广泛表达，被认为是开发针对炎症性肠病（IBD）的新型治疗方法的潜在靶点。计算模拟将巨噬细胞鉴定为针对 IBD 的治疗干预的关键靶标。本研究旨在描述巨噬细胞 PPAR-γ 在 IBD 中发挥有益作用的机制。巨噬细胞特异性 PPAR-γ 缺失显著加重了临床活动和结肠病理学，损害了脾脏和肠系膜淋巴结调节性 T 细胞区室，增加了固有层（LP）CD8+T 细胞的百分比，增加了 LP 巨噬细胞中 CD40、Ly6C 和 Toll 样受体 4（TLR-4）的表面表达，并上调了 IBD 小鼠结肠 IFN-γ、CXCL9、CXCL10、IL-22、IL1RL1、CCR1、细胞因子信号转导抑制因子 3 和 MHC 类 II 的表达。此外，巨噬细胞 PPAR-γ 对于加速吡格列酮介导的葡聚糖硫酸钠（DSS）结肠炎的恢复是必需的，为 PPAR-γ 激动剂在 IBD 中的抗炎作用提供了细胞靶标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6494/3049196/5cd087b96b6a/nihms253584f9.jpg
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