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

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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（AChRs）在调节由聚集IgG（aIgG）和CRP激活的人肥大细胞（MC）中FcγR活性中的作用。 MC是先天和后天免疫界面的关键调节因子，具有丰富的IgG Fc受体（FcγRII），表明其配体IgG和C反应蛋白（CRP）在调节MC活性中的作用。 FcγR依赖的MC功能的胆碱能控制定义不清。用胆碱能药物和FcγR配体（如热聚集的人IgG或纯化的人CRP）进行细胞孵育;化合物48/80，一种已知的利用G蛋白偶联受体的组胺释放剂，被用作MC脱粒的阳性对照。评估nAChR和mAChR拮抗剂（分别为六甲铵和甲基苯丙胺）本身，提高了HMC-1的组胺释放活性，并抑制了对大多数研究的激活剂（咔唑，化合物48/80和在较小程度上aIgG）。为了获得对组胺释放的明显抑制，应将两种阻断剂一起应用于aIgG刺激的细胞。 FcγR介导的HMC-1细胞对CRP的应答对ACh信号减弱的敏感性最低。获得的数据表明ACh参与了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反应密切相关，并可能与FcγR依赖性功能密切相关。所提供的数据表明，AChRs和内源性ACh通过影响功能来参与调节肥大细胞脱粒和组胺释放。化合物48/80和更少的FcγR受体的数量。

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