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人类肠道共生菌中NF-κB调节能力的鉴定

Identification of NF-κB modulation capabilities within human intestinal commensal bacteria.

作者信息

Lakhdari Omar, Tap Julien, Béguet-Crespel Fabienne, Le Roux Karine, de Wouters Tomas, Cultrone Antonietta, Nepelska Malgorzata, Lefèvre Fabrice, Doré Joël, Blottière Hervé M

机构信息

INRA, UMR1319, 78350 Jouy-en-Josas, France.

出版信息

J Biomed Biotechnol. 2011;2011:282356. doi: 10.1155/2011/282356. Epub 2011 Jun 14.

Abstract

The intestinal microbiota plays an important role in modulation of mucosal immune responses. To seek interactions between intestinal epithelial cells (IEC) and commensal bacteria, we screened 49 commensal strains for their capacity to modulate NF-κB. We used HT-29/kb-seap-25 and Caco-2/kb-seap-7 intestinal epithelial cells and monocyte-like THP-1 blue reporter cells to measure effects of commensal bacteria on cellular expression of a reporter system for NF-κB. Bacteria conditioned media (CM) were tested alone or together with an activator of NF-κB to explore its inhibitory potentials. CM from 8 or 10 different commensal species activated NF-κB expression on HT-29 and Caco-2 cells, respectively. On THP-1, CM from all but 5 commensal strains stimulated NF-κB. Upon challenge with TNF-α or IL-1β, some CM prevented induced NF-κB activation, whereas others enhanced it. Interestingly, the enhancing effect of some CM was correlated with the presence of butyrate and propionate. Characterization of the effects of the identified bacteria and their implications in human health awaits further investigations.

摘要

肠道微生物群在调节黏膜免疫反应中发挥着重要作用。为了探寻肠道上皮细胞(IEC)与共生细菌之间的相互作用,我们筛选了49种共生菌株调节核因子κB(NF-κB)的能力。我们使用HT-29/kb-seap-25和Caco-2/kb-seap-7肠道上皮细胞以及单核细胞样THP-1蓝色报告细胞来检测共生细菌对NF-κB报告系统细胞表达的影响。单独测试细菌条件培养基(CM)或与NF-κB激活剂一起测试,以探究其抑制潜力。来自8种或10种不同共生菌的CM分别激活了HT-29和Caco-2细胞上的NF-κB表达。在THP-1细胞上,除5种共生菌株外,其余所有菌株的CM均刺激了NF-κB。在用肿瘤坏死因子-α(TNF-α)或白细胞介素-1β(IL-1β)刺激后,一些CM可阻止诱导的NF-κB激活,而另一些则增强了激活作用。有趣的是,一些CM的增强作用与丁酸盐和丙酸盐的存在有关。已鉴定细菌的作用及其对人类健康的影响有待进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f20c/3134244/1371a9f29931/JBB2011-282356.001.jpg

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