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组胺通过组胺受体 1 诱导尘螨性鼻炎但不诱导哮喘患者的 Th2 激活。

Histamine induces Th2 activation through the histamine receptor 1 in house dust mite rhinitic but not asthmatic patients.

机构信息

L'institut du thorax, INSERM U915, Faculté de médecine, Université de Nantes, Nantes, France.

出版信息

Clin Exp Allergy. 2010 May;40(5):755-62. doi: 10.1111/j.1365-2222.2010.03457.x. Epub 2010 Feb 25.

DOI:10.1111/j.1365-2222.2010.03457.x
PMID:20184607
Abstract

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.

摘要

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即时症状的原因。然而,人们对组胺对 Th2 淋巴细胞的影响知之甚少,而 Th2 淋巴细胞在肥大细胞之前协调过敏反应。

目的

根据是否患有鼻炎或哮喘以及过敏原刺激,我们在屋尘螨(HDM)过敏者中研究了这个问题。

方法

从 15 名鼻炎和 14 名哮喘 HDM 过敏患者和 16 名对照者的外周血单核细胞中培养 Der p 1 或组胺。研究 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 T 细胞细胞因子的产生。使用左西替利嗪评估 H1R 在组胺作用中的作用。

结果

H1R 和 H2R 在哮喘患者的 T 细胞中过度表达,但在鼻炎患者的 T 细胞中没有。Der p 1 增加了来自两个过敏组的 CD4(+)细胞上的 H1R 表达,并降低了对照组的 CD4(+)和 CD8(+)亚群上的 H1R 表达。Der p 1 降低了哮喘患者的 T 细胞 H2R 表达。过敏原增加了两个过敏组的 IL-4 和 IL-13。组胺仅在鼻炎患者中增加 Th2 细胞因子,而左西替利嗪则消除了这种作用。在哮喘患者和对照组中,组胺通过非 H1R 依赖途径降低 T 细胞细胞因子。

结论

在鼻炎中,但不在哮喘中,组胺能够通过依赖 H1R 的正反馈增加 Th2 细胞因子的产生来增加过敏炎症。这一结果部分解释了为什么 H1R 拮抗剂在鼻炎中非常有效,但在哮喘中无效。

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