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细菌通过不依赖Toll样受体(TLR)的机制抑制炎症反应。

Bacterial inhibition of inflammatory responses via TLR-independent mechanisms.

作者信息

Kravchenko Vladimir V, Kaufmann Gunnar F

机构信息

Department of Immunology & Microbial Science, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA, 92037, USA.

出版信息

Cell Microbiol. 2013 Apr;15(4):527-36. doi: 10.1111/cmi.12109. Epub 2013 Feb 5.

Abstract

Identification of cellular processes modulated by microbial organisms that undermine and disarm mammalian host defences against bacterial invaders has been the focus of significant biomedical research. In this microreview we will illustrate the role of bacterial N-acyl homoserine lactones (AHL) as a strategy utilized by Gram-negative bacterial pathogens to enable colonization of the host through AHL-mediated inhibition of inflammation induced via innate immune receptor mechanisms. We will also highlight some of the signalling pathways in which the study of AHL-mediated effects on mammalian cells might lead to the discovery of global underlying principles linking inflammation and immunity to many chronic human diseases, including cancer and obesity.

摘要

鉴定受微生物调节的细胞过程,这些微生物破坏并解除哺乳动物宿主对细菌入侵者的防御,一直是重要生物医学研究的重点。在这篇微型综述中,我们将阐述细菌N-酰基高丝氨酸内酯(AHL)的作用,它是革兰氏阴性细菌病原体采用的一种策略,通过AHL介导抑制经由先天免疫受体机制诱导的炎症,从而实现对宿主的定殖。我们还将强调一些信号通路,在这些通路中,对AHL介导的对哺乳动物细胞影响的研究,可能会发现将炎症和免疫与许多慢性人类疾病(包括癌症和肥胖症)联系起来的全球潜在原理。

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