首页> 外文期刊>FEMS immunology and medical microbiology >Suppressive effects of Bifidobacterium longum on the production of Th2-attracting chemokines induced with T cell-antigen-presenting cell interactions.
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Suppressive effects of Bifidobacterium longum on the production of Th2-attracting chemokines induced with T cell-antigen-presenting cell interactions.

机译:长双歧杆菌对T细胞-抗原呈递细胞相互作用诱导的吸引Th2趋化因子产生的抑制作用。

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摘要

In human trials, Bifidobacterium longum BB536 alleviates subjective symptoms of Japanese cedar pollinosis, an IgE-mediated type I allergy caused by exposure to Japanese cedar, and significantly suppresses the increase of plasma thymus- and activation-regulated chemokine (TARC) associated with pollen dispersion. In the present study, we investigated the suppressive effects of BB536 on the production of T helper type 2 (Th2)-attracting chemokines, such as TARC and macrophage-derived chemokine (MDC), together with the mechanisms of their production. Murine splenocytes were cultured with heat-killed BB536, and the levels of Th2-attracting chemokines in the supernatants were measured. TARC and MDC were produced in cultures without stimulation, and the production was significantly suppressed by BB536. These chemokines were produced by antigen-presenting cells (APCs) of splenocytes stimulated with an anti-CD40 antibody. Furthermore, TARC production was induced with granulocyte macrophage colony-stimulating factor that was produced by T cells and dendritic cells. BB536 suppressed MDC production induced with the anti-CD40 antibody by APCs from the spleen, mesenteric lymph nodes (MLNs) and Peyer's patches, and it suppressed TARC production by APCs from the spleen and MLNs. These results indicate that BB536 suppresses the production of Th2-attracting chemokines induced by the T cell-APC interaction, suggesting a novel mechanism for alleviating symptoms of allergic disorders by probiotics.
机译:在人体试验中,长双歧杆菌BB536缓解了日本雪松花粉病的主观症状,这是由暴露于日本雪松引起的IgE介导的I型过敏,并显着抑制了与花粉分散有关的血浆胸腺和活化调节趋化因子(TARC)的增加。在本研究中,我们研究了BB536对2型T辅助吸引(Th2)趋化因子如TARC和巨噬细胞衍生趋化因子(MDC)的抑制作用,以及它们的产生机理。用热灭活的BB536培养鼠脾细胞,并测量上清液中Th2吸引趋化因子的水平。 TARC和MDC产生于无刺激的培养物中,BB536显着抑制了产生。这些趋化因子是由抗CD40抗体刺激的脾细胞的抗原呈递细胞(APC)产生的。此外,由T细胞和树突状细胞产生的粒细胞巨噬细胞集落刺激因子诱导TARC产生。 BB536抑制了抗CD40抗体诱导的APC从脾脏,肠系膜淋巴结(MLN)和Peyer斑块诱导的MDC产生,并且它抑制了APC脾和MLN产生的TARC产生。这些结果表明BB536抑制了由T细胞-APC相互作用诱导的吸引Th2的趋化因子的产生,提示了益生菌减轻过敏性疾病症状的新机制。

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