Mast cells, which express the high-affinity IgE receptor (FcεRI) on their surface, play a crucial role in inducing allergic inflammation. Since mast cells are activated by crosslinking of FcεRI with IgE and allergens, the cell surface expression level of FcεRI is an important factor in determining the sensitivity to allergens. Recently, the involvement of gut microbiota in the prevalence and regulation of allergy has attracted attention but the precise underlying mechanisms are not fully understood. In this study, the effect of intestinal bacteria on cell surface expression of FcεRI was examined. Bacteroides acidifaciens type A 43 specifically suppressed cell surface expression of FcεRI on mouse bone marrow-derived mast cells (BMMCs) without reduction in FcεRI α and β-chain mRNA and total protein expression. The suppressive effect required sustained exposure to this bacterium, with a corresponding reduction in Erk activation. Inhibition of Erk decreased cell surface distribution of FcεRI in BMMCs, at least in part, through facilitated endocytosis of FcεRI. These results indicate that B. acidifaciens type A 43 suppresses cell surface expression of FcεRI on mast cells in a post-translational manner via inhibition of Erk. The suppression of FcεRI expression on mast cells by specific bacteria might be the underlying mechanism involved in the regulation of allergy by gut microbiota.

肥大细胞表面表达高亲和力 IgE 受体 (FcεRI)，在诱发过敏性炎症中发挥着至关重要的作用。由于肥大细胞是通过 FcεRI 与 IgE 和过敏原交联而激活的，因此 FcεRI 的细胞表面表达水平是决定对过敏原敏感性的重要因素。最近，肠道微生物群参与过敏的流行和调节引起了人们的关注，但其确切的潜在机制尚不完全清楚。在本研究中，检测了肠道细菌对 FcεRI 细胞表面表达的影响。 A 型拟杆菌43 特异性抑制小鼠骨髓源性肥大细胞 (BMMC) 上 FcεRI 的细胞表面表达，而不降低 FcεRI α 和 β 链 mRNA 以及总蛋白表达。抑制作用需要持续接触这种细菌，同时 Erk 激活也会相应减少。 Erk 的抑制至少部分地通过促进 FcεRI 的内吞作用减少了 BMMC 中 FcεRI 的细胞表面分布。这些结果表明，A型酸芽孢杆菌43通过抑制Erk以翻译后方式抑制肥大细胞上FcεRI的细胞表面表达。特定细菌对肥大细胞上 FcεRI 表达的抑制可能是肠道微生物群调节过敏的潜在机制。