The prevalence of atopic diseases has been steadily increasing since the mid 20th century, a rise that has been linked to modern hygienic lifestyles that limit exposure to microbes and immune system maturation. Overactive type 2 CD4+ helper T (Th2) cells are known to be closely associated with atopy and represent a key target for treatment. In this study, we report that the ammonia oxidizing bacteria (AOB) Nitrosomonas eutropha D23, an environmental microbe that is not associated with human pathology, effectively suppresses the polarization of Th2 cells and production of Th2-associated cytokines (IL-5, IL-13, & IL-4) by human peripheral blood mononuclear cells (PBMC). We show that AOB inhibit Th2 cell polarization not through Th1- mediated suppression, but rather through an IL-10-mediated mechanism that interferes with the activation of dendritic cells, as evidenced by a reduction in Major Histocompatibility Complex Class II (MHC II) and CD86 expression following AOB treatment. This is the first report of immunomodulatory properties of AOB and supports the development of AOB as a potential therapeutic for atopic diseases.

中文翻译：

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氨氧化细菌Nitrosomonas eutropha D23通过IL-10介导的对树突状细胞活化的干扰，阻断了T辅助细胞2的极化

自20世纪中叶以来，特应性疾病的发病率一直在稳步上升，这一上升与现代卫生生活方式有关，这种生活方式限制了微生物的接触和免疫系统的成熟。已知过度活跃的2型CD4 +辅助性T（Th2）细胞与特应性疾病密切相关，是治疗的关键靶点。在这项研究中，我们报告说，氨氧化细菌（AOB）亚硝化单胞菌D23，一种与人类病理学无关的环境微生物，可有效抑制Th2细胞的极化和Th2相关细胞因子（IL-5，IL- 13，IL-4）被人类外周血单核细胞（PBMC）所吸收。我们显示AOB不会通过Th1介导的抑制作用来抑制Th2细胞极化，而是通过IL-10介导的机制来干扰树突状细胞的激活，这一点可通过AOB治疗后II类主要组织相容性复合物（MHC II）和CD86表达的降低来证明。这是AOB免疫调节特性的首次报道，并支持AOB作为特应性疾病的潜在治疗剂的发展。