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鼠树突状细胞过继转移对鼠哮喘中鼠李糖乳杆菌作用的影响。

Effects of Lactobacillus rhamnosus on asthma with an adoptive transfer of dendritic cells in mice.

机构信息

Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea.

出版信息

J Appl Microbiol. 2013 Sep;115(3):872-9. doi: 10.1111/jam.12268. Epub 2013 Jun 24.

Abstract

AIM

This study was designed to investigate whether the protective effects of Lactobacillus rhamnosus (Lcr35) on allergic asthma are associated with the adoptive transfer of dendritic cells (DCs) and regulatory T cells (Tregs), using a mouse experimental model of asthma.

METHODS AND RESULTS

BALB/c mice were orally administered Lcr35 or intravenously treated with in vivo Lcr35-treated DCs daily and were then sensitized and challenged with ovalbumin (OVA) in accordance with a model of asthma protocol. Both the oral application of Lcr35 and intravenous administration of Lcr35-treated DCs suppressed all aspects of the asthmatic response, including bronchial hyperresponsiveness (BHR), total cell counts in the bronchoalveolar lavage (BAL) fluid, the production of OVA-specificimmunoglobulin E (IgE), and pulmonary eosinophilic inflammation. The mechanism of action of Lcr35 is related to Tregs, which suppress the Th2 response in the respiratory organs, and this is mediated by DCs in the mouse model of asthma.

CONCLUSIONS

These results confirm that the mechanism underlying the effects of Lcr35 on asthma involves the adoptive transfer of DCs.

SIGNIFICANCE AND IMPACT OF THE STUDY

This finding broadens the possibility that Lcr35 has potential as an alternative therapeutic approach to the treatment of human asthma.

摘要

目的

本研究旨在通过哮喘小鼠模型,探讨鼠李糖乳杆菌(Lcr35)对过敏性哮喘的保护作用是否与树突状细胞(DCs)和调节性 T 细胞(Tregs)的过继转移有关。

方法和结果

BALB/c 小鼠每日口服 Lcr35 或静脉内给予体内 Lcr35 处理的 DCs,并按照哮喘模型方案用卵清蛋白(OVA)致敏和激发。Lcr35 的口服应用和 Lcr35 处理的 DC 的静脉内给药均抑制哮喘反应的各个方面,包括支气管高反应性(BHR)、支气管肺泡灌洗液(BAL)中的总细胞计数、OVA 特异性免疫球蛋白 E(IgE)的产生和肺嗜酸性粒细胞炎症。Lcr35 的作用机制与 Tregs 有关,Tregs 抑制呼吸道中的 Th2 反应,这在哮喘小鼠模型中是由 DCs 介导的。

结论

这些结果证实,Lcr35 对哮喘的作用机制涉及 DCs 的过继转移。

研究的意义和影响

这一发现拓宽了 Lcr35 作为治疗人类哮喘的一种替代治疗方法的可能性。

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