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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Recognition of the microbiota by Nod2 contributes to the oral adjuvant activity of cholera toxin through the induction of interleukin-1 beta
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Recognition of the microbiota by Nod2 contributes to the oral adjuvant activity of cholera toxin through the induction of interleukin-1 beta

机译：NOD2识别微生物群通过诱导白细胞介素-1β的诱导有助于霍乱毒素的口服助辅助活性

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The role of symbiotic bacteria in the development of antigen-specific immunity remains poorly understood. Previous studies showed that sensing of symbiotic bacteria by nucleotide-binding oligomerization domain-containing protein 2 (Nod2) regulates antibody responses in response to nasal immunization with antigen and cholera toxin (CT). In this study, we examined the role of the microbiota in the adjuvant activity of CT induced after oral immunization with antigen. Germ-free (GF) mice showed impaired production of antibody responses and T-cell-specific cytokines after oral immunization when compared with that observed in conventionally raised mice. Similar to GF mice, Nod2-deficient mice showed reduced humoral responses upon oral immunization with antigen and CT. Treatment with CT enhanced the production of interleukin-1 beta (IL-1 beta), but not tumor necrosis factor-alpha or IL-12p40, induced by stimulation of dendritic cells with muramyl dipeptide, the Nod2 ligand. Mechanistically, the enhanced production of IL-1 beta induced by muramyl dipeptide and CT stimulation required Nod2 and was mediated by both increased synthesis of pro-IL-1 beta and caspase-1 activation. Furthermore, antigen-specific antibody and cytokine responses induced by CT were impaired in orally immunized IL-1 beta-deficient mice. Collectively, our results indicate that Nod2 stimulation by symbiotic bacteria contributes to optimal CT-mediated antigen-specific oral vaccination through the induction of IL-1 beta production.
机译：共生细菌在抗原特异性免疫发育的作用仍然明显差不多。以前的研究表明，含有核苷酸结合寡聚化结构域的蛋白2（NOD2）的对共生细菌的感测调节抗体反应，响应抗原和霍乱毒素（CT）。在这项研究中，我们研究了微生物群在用抗原口服免疫后CT诱导的CT的佐剂活性中的作用。与在常规升高的小鼠中观察到的比较时，无菌（GF）小鼠显示出在口服免疫后的抗体反应和特异性特异性细胞因子。与GF小鼠类似，Nod2缺陷小鼠在用抗原和CT的口服免疫时表现出减少体液反应。用CT治疗增强了白细胞介素-1β（IL-1β）的产生，但不是通过刺激与蛋白质二肽的树突细胞，Nod2配体刺激肿瘤坏死因子-α或IL-12P40的产生。机械地，由Muramyl Dipeptide和CT刺激诱导的IL-1β的增强的产生，并通过增加Pro-IL-1β和Caspase-1活化的增加来介导。此外，CT诱导的抗原特异性抗体和细胞因子反应在口服免疫的IL-1β缺陷小鼠中受到损害。我们的结果表明，通过诱导IL-1β生产，共生细菌的NOD2刺激有助于最佳的CT介导的抗原特异性口腔疫苗接种。

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