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首页> 外文期刊>Clinical and experimental allergy : >Histamine induces Th2 activation through the histamine receptor 1 in house dust mite rhinitic but not asthmatic patients.
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Histamine induces Th2 activation through the histamine receptor 1 in house dust mite rhinitic but not asthmatic patients.

机译：组胺通过鼻内尘螨而非哮喘患者的组胺受体1诱导Th2活化。

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BACKGROUND: Effects of mast cell-released histamine on smooth muscle and endothelial cells are considered as responsible of immediate symptoms of anaphylaxis. However, little is known about histamine effects on Th2 lymphocytes, which orchestrate the allergic reaction upstream of mast cells. OBJECTIVE: We addressed this question in house dust mite (HDM) allergics, according to the presence of rhinitis or asthma and allergen stimulation. METHODS: Peripheral blood mononuclear cell from 15 rhinitic and 14 asthmatic HDM-allergic subjects and 16 controls were cultured with Der p 1 or histamine. The effect of Der p 1 on histamine receptor (H1R and H2R) expression was studied. T-cell cytokine production was studied upon Der p 1 or histamine stimulation. The role of H1R in histamine effects was assessed with levocetirizine. RESULTS: H1R and H2R are overexpressed on T cells from asthmatic but not from rhinitic subjects. Der p 1 increases H1R expression on CD4(+) cells from both allergic groups, and decreases it in controls, on CD4(+) and CD8(+) subsets. Der p 1 decreases T-cell H2R expression in asthmatics. Allergen increases IL-4 and IL-13 in both allergic groups. Histamine increases Th2 cytokines in rhinitics only, and levocetirizine abolishes this effect. In asthmatics and controls, histamine decreases T-cell cytokines through a non-H1R dependent pathway. CONCLUSION: In rhinitis but not in asthma, histamine is able to increase allergic inflammation by increasing Th2 cytokine production in a positive feedback dependent on H1R. This result could explain in part why H1R antagonists, are very efficient in rhinitis, but not in asthma.
机译：背景：肥大细胞释放的组胺对平滑肌和内皮细胞的影响被认为是过敏反应的直接症状。但是，关于组胺对Th2淋巴细胞的影响知之甚少，Th2淋巴细胞协调肥大细胞上游的过敏反应。目的：根据存在的鼻炎或哮喘以及过敏原刺激，我们在室内尘螨（HDM）过敏症中解决了这个问题。方法：用Der p 1或组胺培养15名鼻炎和14名哮喘HDM过敏性受试者以及16名对照的外周血单个核细胞。研究了Der p 1对组胺受体（H1R和H2R）表达的影响。在Der p 1或组胺刺激下研究了T细胞细胞因子的产生。用左西替利嗪评估了H1R在组胺作用中的作用。结果：哮喘和哮喘患者的T细胞中H1R和H2R过表达。 Der p 1增加了两个过敏组的CD4（+）细胞上的H1R表达，而在对照组中CD4（+）和CD8（+）子集上的H1R表达降低。 Der p 1降低哮喘患者的T细胞H2R表达。在两个过敏组中，过敏原均会增加IL-4和IL-13。组胺仅增加鼻炎患者的Th2细胞因子，而左西替利嗪则取消了这种作用。在哮喘患者和对照组中，组胺通过非H1R依赖性途径减少T细胞细胞因子。结论：在鼻炎而非哮喘中，组胺能够通过依赖于H1R的正反馈增加Th2细胞因子的产生来增加过敏性炎症。这个结果可以部分解释为什么H1R拮抗剂在鼻炎中非常有效，而在哮喘中却没有。

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