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肥大细胞作为宿主免疫防御革兰氏阴性菌的关键效应因子。

Mast cells as critical effectors of host immune defense against Gram-negative bacteria.

机构信息

Department of Oral Biochemistry, Graduate School of Medical and Dental Sciences, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8544, Japan.

出版信息

Curr Med Chem. 2012;19(10):1432-42. doi: 10.2174/092986712799828319.

Abstract

Mast cells are best known as central effector cells in IgE-mediated type I allergic diseases including asthma and hay fever. An increasing amount of evidence, however, has demonstrated that mast cells are sentinel cells playing a critical role in host defense against invading microbes. Mast cells are located immediately beneath the epithelial surfaces exposed to the outer environment, such as genitourinary and gastrointestinal tracts, skin, and airways. This review discusses recent studies on the critical roles of mast cells in host defense against Gram-negative bacterial infection. Mast cells are equipped with multiple receptors detecting the invading Gram-negative bacteria in both direct (opsonin-independent) and indirect (opsonin-dependent) mechanisms. The former includes Toll-like receptors (TLRs), CD48, and nucleotide-binding oligomerization (NOD) proteins, while the latter includes Fcγ receptors (FcγRs) and complement receptors. In addition to the detecting systems, mast cells are also armed with versatile tools to combat and kill Gram-negative bacteria. In response to the recognition of the Gram-negative bacterial infection, mast cells secrete various types of mediators which either regulate host immune system or directly attack the bacteria. Mast cells can also phagocytize and subsequently display the bacterial antigens on their cell surfaces. Moreover, recent findings have revealed the formation of extra-cellular traps by mast cells. Finally this review will especially focus on recent findings on LPS signaling in mast cells, both the functional outcome and the molecular mechanisms.

摘要

肥大细胞作为 IgE 介导的 I 型过敏性疾病(包括哮喘和花粉热)的主要效应细胞而广为人知。然而,越来越多的证据表明,肥大细胞作为哨兵细胞,在宿主抵御入侵微生物的防御中发挥着关键作用。肥大细胞位于暴露于外部环境的上皮表面(如泌尿生殖道、胃肠道、皮肤和气道)的下方。本文综述了肥大细胞在宿主防御革兰氏阴性菌感染中的关键作用的最新研究进展。肥大细胞配备了多种受体,可以通过直接(非调理素依赖)和间接(调理素依赖)机制检测入侵的革兰氏阴性菌。前者包括 Toll 样受体 (TLR)、CD48 和核苷酸结合寡聚化 (NOD) 蛋白,而后者包括 Fcγ 受体 (FcγR) 和补体受体。除了检测系统外,肥大细胞还拥有多种工具来对抗和杀死革兰氏阴性菌。在识别革兰氏阴性菌感染后,肥大细胞会分泌各种类型的介质,这些介质可以调节宿主免疫系统或直接攻击细菌。肥大细胞还可以吞噬并随后在其细胞表面展示细菌抗原。此外,最近的研究结果揭示了肥大细胞形成细胞外陷阱的能力。最后,本文将特别关注肥大细胞中 LPS 信号转导的最新发现,包括功能结果和分子机制。

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