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裂解和破碎的BGN4细胞可促进脂多糖刺激的RAW 264.7细胞的抗炎活性。

Lysed and disrupted BGN4 cells promote anti-inflammatory activities in lipopolysaccharide-stimulated RAW 264.7 cells.

作者信息

Lee Nayeon, Lee Soomin, Jang Se-Won, Shin Hee Soon, Park Jong-Hyun, Park Myeong Soo, Lee Byung-Hoo

机构信息

Department of Food Science and Biotechnology, Gachon University, Seongnam 13120, Republic of Korea.

Korea Food Research Institute, Wanju 55365, Republic of Korea.

出版信息

Saudi J Biol Sci. 2021 Sep;28(9):5115-5118. doi: 10.1016/j.sjbs.2021.05.028. Epub 2021 May 20.

DOI:10.1016/j.sjbs.2021.05.028
PMID:34466089
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8381009/
Abstract

BGN4 has been shown to improve the immune system by regulating interleukin (IL)-6 in RAW 264.7 macrophage cells. In this study, the dead cells of BGN4 were produced by enzymatic and physical processing to enhance the inhibition properties of pro-inflammatory cytokines using lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Notably, the secretion levels of cytokines such as interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α were decreased by the cell-wall disrupted extracts compared to heat-killed cells. The result suggests that the exposed interior-surface of BGN4 has a potential ability to regulate the immune-responses in the gastrointestinal tract due to major substances in inside-cell wall such as peptidoglycan and teichoic acids. In conclusion, the lysed and disrupted cells from the inside out of BGN4 have anti-inflammatory properties as paraprobiotic agents to control chronic inflammatory related-diseases.

摘要

已证明BGN4可通过调节RAW 264.7巨噬细胞中的白细胞介素(IL)-6来改善免疫系统。在本研究中,通过酶促和物理处理产生BGN4的死细胞,以增强使用脂多糖(LPS)刺激的RAW 264.7细胞对促炎细胞因子的抑制特性。值得注意的是,与热杀死的细胞相比,细胞壁破坏提取物降低了白细胞介素(IL)-1β、IL-6、IL-8和肿瘤坏死因子(TNF)-α等细胞因子的分泌水平。结果表明,由于细胞壁内部的主要物质如肽聚糖和磷壁酸,BGN4暴露的内表面具有调节胃肠道免疫反应的潜在能力。总之,从内到外裂解和破坏的BGN4细胞具有作为副益生菌控制慢性炎症相关疾病的抗炎特性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4612/8381009/c782fd4ae7da/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4612/8381009/4e5be7d18b64/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4612/8381009/c782fd4ae7da/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4612/8381009/4e5be7d18b64/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4612/8381009/c782fd4ae7da/gr2.jpg

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