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伊拉克蜂胶通过自噬增加铜绿假单胞菌感染后 IL-1β 和 NLRC4 的降解。

Iraqi propolis increases degradation of IL-1β and NLRC4 by autophagy following Pseudomonas aeruginosa infection.

机构信息

Division of Biotechnology, Department of Applied Science, University of Technology, Baghdad, Iraq.

Division of Biotechnology, Department of Applied Science, University of Technology, Baghdad, Iraq.

出版信息

Microbes Infect. 2018 Feb;20(2):89-100. doi: 10.1016/j.micinf.2017.10.007. Epub 2017 Nov 8.

DOI:10.1016/j.micinf.2017.10.007
PMID:29104144
Abstract

Autophagy is a cellular process for maintaining cellular homeostasis. This process can be induced by different factors, such as immune stimuli and pathogen-associated molecules. Autophagy has an important role in the control of IL-1β secretion by macrophages and other cell types. In present study, we describe a novel role for Iraqi propolis affecting autophagy in controlling the secretion of IL-1β in bone-marrow macrophages (BMDMs). After infection with Pseudomonas aeruginosa in the presence of propolis, the degradation of IL-1β was induced, and the activity of inflammasome was reduced. Iraqi propolis-induced autophagy in in vitro and in vivo models decreased the levels of IL-1β and caspase-1. Results indicated that IL-1β pathway production is regulated by autophagy via two different novel mechanisms, namely, regulation of the activation of NLRC4 inflammasome and IL-1β targeting for lysosomal degradation.

摘要

自噬是一种维持细胞内稳态的细胞过程。这个过程可以被不同的因素诱导,例如免疫刺激和病原体相关分子。自噬在控制巨噬细胞和其他细胞类型中 IL-1β 的分泌方面起着重要作用。在本研究中,我们描述了伊拉克蜂胶在控制骨髓巨噬细胞(BMDM)中 IL-1β 分泌方面的一种新的自噬作用。在存在蜂胶的情况下感染铜绿假单胞菌后,诱导了 IL-1β 的降解,并且炎症小体的活性降低。在体外和体内模型中,伊拉克蜂胶诱导的自噬降低了 IL-1β 和 caspase-1 的水平。结果表明,自噬通过两种不同的新机制调节 IL-1β 途径的产生,即 NLRC4 炎症小体的激活调节和 IL-1β 靶向溶酶体降解。

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