Department of Laboratory Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.
NPJ Biofilms Microbiomes. 2024 Sep 12;10(1):84. doi: 10.1038/s41522-024-00563-z.
The role of mast cells (MCs) in ulcerative colitis (UC) development is controversial. FcεRI, the IgE high-affinity receptor, is known to activate MCs. However, its role in UC remains unclear. In our study, Anti-FcεRI showed highly diagnostic value for UC. FcεRIα knockout in mice ameliorated DSS-induced colitis in a gut microbiota-dependent manner. Increased Lactobacillus abundance in FcεRIα deficient mice showed strongly correlation with the remission of colitis. RNA sequencing indicated activation of the NLRP6 inflammasome pathway in FcεRIα knockout mice. Additionally, Lactobacillus plantarum supplementation protected against inflammatory injury and goblet cell loss, with activation of the NLRP6 inflammasome during colitis. Notably, this effect was absent when the strain is unable to produce lactic acid. In summary, colitis was mitigated in FcεRIα deficient mice, which may be attributed to the increased abundance of Lactobacillus. These findings contribute to a better understanding of the relationship between allergic reactions, microbiota, and colitis.
肥大细胞（MCs）在溃疡性结肠炎（UC）发展中的作用存在争议。FcεRI，即 IgE 高亲和力受体，已知可激活 MCs。然而，其在 UC 中的作用仍不清楚。在我们的研究中，抗 FcεRI 对 UC 具有高度诊断价值。FcεRIα 敲除小鼠在肠道微生物群依赖性方式下减轻了 DSS 诱导的结肠炎。FcεRIα 缺陷小鼠中乳杆菌丰度的增加与结肠炎的缓解呈强烈相关性。RNA 测序表明，FcεRIα 敲除小鼠中 NLRP6 炎性小体途径被激活。此外，植物乳杆菌补充可预防炎症损伤和杯状细胞丢失，并在结肠炎期间激活 NLRP6 炎性小体。值得注意的是，当该菌株无法产生乳酸时，这种作用就不存在了。总之，FcεRIα 缺陷小鼠中的结肠炎得到缓解，这可能归因于乳杆菌丰度的增加。这些发现有助于更好地理解过敏反应、微生物群和结肠炎之间的关系。
