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巨噬细胞耗竭可预防香烟烟雾诱导的小鼠结肠和肺部炎症反应。

Macrophage Depletion Protects against Cigarette Smoke-Induced Inflammatory Response in the Mouse Colon and Lung.

作者信息

Lim Dahae, Kim Woogyeong, Lee Chanju, Bae Hyunsu, Kim Jinju

机构信息

Department of Korean Physiology, College of Pharmacy, Kyung Hee University, Seoul, South Korea.

Department of Science in Korean Medicine, Kyung Hee University, Seoul, South Korea.

出版信息

Front Physiol. 2018 Feb 12;9:47. doi: 10.3389/fphys.2018.00047. eCollection 2018.

DOI:10.3389/fphys.2018.00047
PMID:29483875
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5816061/
Abstract

Cigarette smoke (CS) is considered as a major risk factor for pulmonary and intestinal inflammation. CS leads to macrophage infiltration in the mucosae of the lung and colon, inducing the uncontrolled secretion of inflammatory mediators, and thus promoting inflammatory response. In this study, we investigated whether macrophage depletion modulates cigarette smoke (CS)-induced inflammatory response in both the lung and colon. The mice were exposed to CS for 30 min, after which they were rested in a fresh air environment for 30 min. The total duration of exposure to CS was 2 h per day for 4 weeks. Macrophage depletion state was made with the injection of clodronate containing liposome. Individual body weights were measured twice a week, and the mice were sacrificed on day 28. Hematoxylin and eosin (H&E) staining was performed in the lung and colon tissue to determine histological changes. Inflammatory mediators' synthesis was analyzed using ELISA and western blotting. Clodronate liposome treatment ameliorated pathological changes associated with the infiltration of immune cells in the lung and colon. Also, clodronate liposome injected mice showed significantly lower level of inflammatory mediators, including cytokines and chemokine and proteases. Our results indicated that macrophage depletion by clodronate liposome treatment attenuates CS-induced inflammatory response in both the lung and colon.

摘要

香烟烟雾(CS)被认为是肺部和肠道炎症的主要危险因素。CS会导致巨噬细胞浸润到肺和结肠的黏膜中,诱导炎症介质的失控分泌,从而促进炎症反应。在本研究中,我们调查了巨噬细胞耗竭是否会调节香烟烟雾(CS)诱导的肺和结肠炎症反应。将小鼠暴露于CS中30分钟,之后让它们在新鲜空气环境中休息30分钟。每天暴露于CS的总时长为2小时,持续4周。通过注射含氯膦酸盐的脂质体使巨噬细胞处于耗竭状态。每周测量两次个体体重,并在第28天处死小鼠。对肺和结肠组织进行苏木精和伊红(H&E)染色以确定组织学变化。使用酶联免疫吸附测定(ELISA)和蛋白质印迹法分析炎症介质的合成。氯膦酸盐脂质体处理改善了与肺和结肠中免疫细胞浸润相关的病理变化。此外,注射氯膦酸盐脂质体的小鼠显示出炎症介质水平显著降低,包括细胞因子、趋化因子和蛋白酶。我们的结果表明,通过氯膦酸盐脂质体处理使巨噬细胞耗竭可减轻CS诱导的肺和结肠炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83e9/5816061/4c220d1a514e/fphys-09-00047-g0013.jpg
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