Link between mast cells and bacteria: Antimicrobial defense, function and regulation by cytokines
Link between mast cells and bacteria: Antimicrobial defense, function and regulation by cytokines
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DOI：
10.1016/j.mehy.2017.06.018
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发表时间：
2017-09-01
影响因子：
4.7
通讯作者：
Theoharides, Theoharis C.
中科院分区：
文献类型：
--
作者：
Conti, Pio;Carinci, Francesco;Theoharides, Theoharis C.
细菌及其产物，例如LPS，作用于肥大细胞（MC）以诱导多种细胞因子的分泌，包括IL-1、TNF、IL-18和IL-33，其可以在感染组织的部位给药。抗原结合IgE交联肥大细胞上的Fc ε RI涉及PKC δ、ERK、酪氨酸激酶（Syk和林恩）和丝裂原活化蛋白激酶（MAPK）的产生和活化，诱导化学介质的释放，所述化学介质引起炎症和过敏反应。其他刺激，包括细胞因子、神经肽、化学和物理激活剂，也可以作用于MC以释放过多的炎性化合物。活化的MC产生广谱的炎性细胞因子、趋化因子、脂质化合物和血管活性胺，所有这些都参与免疫应答。通过产生TNF，MC具有抗菌防御和保护功能;而病原菌及其产物，如LPS，通过MC活化具有炎症反应。LPS结合TLR 4产生MC一代IL-1家族成员，和趋化因子，这可能会在感染部位招募炎性细胞;而在Kit（w/w-v）小鼠，其中MC是遗传缺乏，炎症效应是不存在的。我们报告的第一次MC和细菌之间的联系，强调炎症细胞因子/趋化因子的介导。我们可以得出结论，肥大细胞对抗细菌，它们的免疫反应完美地整合在免疫网络中。我们希望对微生物和肥大细胞相互作用的理解能够导致与微生物耐药性相关的更有效的治疗开发。(C)2017爱思唯尔有限公司版权所有
Bacteria and their products, such as LPS, act on mast cells (MCs) to induce the secretion of multiple cytokines, including IL-1, TNF, IL-18 and IL-33, which can be dosed in the site of infected tissues. Antigen-binding IgE cross-links Fc epsilon RI on mast cells involves the generation and activation of PKC delta, ERK, tyrosine kinases (Syk and Lyn) and mitogen-activated protein kinases (MAPKs), inducing the release of chemical mediators which provoke inflammation and hypersensitive reaction. Other stimuli, including, cytokines, neuropeptides, chemical and physical activators, can also act on MCs to release a plethora of inflammatory compounds. Activated MCs produce a broad spectrum of inflammatory cytokines, chemokines, lipid compounds and vasoactive amines, all involved in immune response. By producing TNF, MCs have an antibacterial defense and a protective function; while pathogenic bacteria and their products, such as LPS, have an inflammatory response through MC activation. LPS binding TLR4 produce MC generation IL-1 family members, and chemokines, which may recruit inflammatory cells at the infection site; whereas in Kit(w/w-v) mice, where MCs are genetically absent, the inflammatory effect is not present.We report for the first time a link between MCs and bacteria emphasizing the mediation of inflammatory cytokines/chemokines. We can conclude that mast cells fight bacteria, and their immune response is perfectly integrated in the immune network. We hope that the understanding of microbial and mast cell interaction leads to more efficient therapeutic development in relation to microbial resistance. (C) 2017 Elsevier Ltd. All rights reserved.