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幽门螺杆菌、哮喘与过敏

Helicobacter pylori, asthma and allergy.

作者信息

D'Elios Mario Milco, Codolo Gaia, Amedei Amedeo, Mazzi Paola, Berton Giorgio, Zanotti Giuseppe, Del Prete Gianfranco, de Bernard Marina

机构信息

Department of Internal Medicine, University of Florence, Florence, Italy.

出版信息

FEMS Immunol Med Microbiol. 2009 Jun;56(1):1-8. doi: 10.1111/j.1574-695X.2009.00537.x. Epub 2009 Feb 10.

DOI:10.1111/j.1574-695X.2009.00537.x
PMID:19220467
Abstract

Bronchial asthma and allergic diseases are orchestrated by T-cells producing T-helper type 2 (Th2) cytokines, such as interleukin-4 (IL-4) and IL-5, and are inhibited by Th1 responses. Helicobacter pylori has chronically infected the human population for c. 100,000 years and preferentially elicits a Th1 mucosal immune response with the production of interferon-gamma and IL-12. Among several bacterial factors, the neutrophil-activating protein of H. pylori (HP-NAP) not only plays a key role in driving Th1 inflammation but it is also able to inhibit Th2 responses in vitro and in vivo in allergic bronchial asthma, in humans and mice. Both systemic and mucosal administrations of HP-NAP are successful in reducing eosinophilia, immunoglobulin E and systemic Th2 cytokines at the bronchial level. Thus, these results identify HP-NAP as a candidate for novel strategies for the prevention and treatment of allergic diseases.

摘要

支气管哮喘和过敏性疾病是由产生2型辅助性T细胞(Th2)细胞因子(如白细胞介素-4(IL-4)和IL-5)的T细胞所调控,且受到Th1反应的抑制。幽门螺杆菌已在人类群体中慢性感染约10万年,并优先引发产生干扰素-γ和IL-12的Th1黏膜免疫反应。在多种细菌因素中,幽门螺杆菌的中性粒细胞激活蛋白(HP-NAP)不仅在驱动Th1炎症中起关键作用,而且在体外和体内均能抑制人类和小鼠过敏性支气管哮喘中的Th2反应。全身和黏膜给予HP-NAP均可成功降低支气管水平的嗜酸性粒细胞增多、免疫球蛋白E和全身Th2细胞因子。因此,这些结果表明HP-NAP是预防和治疗过敏性疾病新策略的一个候选物。

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