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首页> 外文期刊>Life sciences >The influence of cholinergic agents on histamine release from HMC-1 human mast cell line stimulated with IgG, C-reactive protein and compound 48/80.
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The influence of cholinergic agents on histamine release from HMC-1 human mast cell line stimulated with IgG, C-reactive protein and compound 48/80.

机译：用IgG，C-反应蛋白和化合物48/80刺激HMC-1人肥大细胞系中胆碱能药物对组胺释放的影响。

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摘要

The aim of this work is to study the role of acetylcholine (ACh) receptors (AChRs) in the regulation of FcγR activity in human mast cells (MC) activated by aggregated IgG (aIgG) and CRP. MC, the key regulators at the interface of innate and acquired immunity, have abundant Fc receptors for IgG (FcγRII) which indicate the role of their ligands, IgG and C-reactive protein (CRP), in regulating MC activity. Cholinergic control of FcγR-dependent MC functions is poorly defined.HMC-1 culture of human MC; cell incubations with cholinergic drugs and FcγR ligands such as heat aggregated human IgG or purified human CRP; compound 48/80, a known histamine liberator employing G protein-coupled receptors, was used as a positive control of MC degranulation; assessment of histamine release.Both nAChR and mAChR antagonists (hexamethonium and methacine, respectively), per se, elevated histamine-releasing activity of the HMC-1 and suppressed the MC responses to most of investigated activators (carbachol, compound 48/80, and to a lesser extent aIgG). Two blockers together should be applied to aIgG-stimulated cells in order to obtain appreciable suppression of histamine release. The FcγR-mediated HMC-1 cell response to CRP was the least sensitive to attenuation by ACh signaling.The data obtained suggest the involvement of ACh in the functioning of other receptor systems. Our results indicate that AChRs are closely associated with G protein-coupled receptor-induced reactions of MC and optionally with FcγR-dependent functions.The data presented demonstrate that AChRs and endogenous ACh are involved in regulating mast cell degranulation and histamine release by affecting the functions of receptors to compound 48/80 and, less, FcγRs.
机译：这项工作的目的是研究乙酰胆碱（ACH）受体（ACHR）在通过聚集的IgG（AIGG）和CRP活化的人肥大细胞（MC）中的FcγR活性调节中的作用。 MC，在先天和获得的免疫接口处的关键稳压器具有丰富的IgG（FCγRII）的Fc受体，其表明它们的配体，IgG和C反应蛋白（CRP）在调节MC活性方面的作用。依赖于FCγR依赖性MC功能的胆碱能控制差异很差。HMC-1人MC培养物;细胞孵育与胆碱能药物和FcγR配体，如热聚合人IgG或纯化的人CRP;化合物48/80，一种使用G蛋白偶联受体的已知的组胺释放剂，用作MC脱粒的阳性对照;分析组胺释放的评估。结肠和阵列拮抗剂（分别为HMC-1的HMC-1的升高的组胺释放活性，并抑制了对大多数研究的活化剂（Carbachol，化合物48/80和在较小的程度上aigg）。两个受体阻断剂应施加到AIGG刺激的细胞中，以获得可明显的组胺释放的抑制。对CRP的FCγR介导的HMC-1细胞对CRP的响应是通过ACH信号传导的衰减最小敏感性。该数据表明ACH参与其他受体系统的功能。我们的结果表明，ACHRs与G蛋白偶联受体诱导的MC和任选地具有FcγR依赖性功能的反应密切相关。提出的数据证明ACHR和内源性ACH通过影响功能来调节桅杆细胞脱粒和组胺释放。化合物48/80的受体，较少，FcγRS。

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