Objective

To provide a concise summary of the current literature regarding gastrointestinal immunopathology of food protein–induced enterocolitis syndrome (FPIES) and other non-immunoglobulin E (IgE)–mediated food allergic diseases.

Data Sources

Data were extracted from PubMed, MEDLINE, and ScienceDirect databases.

Study Selections

Original articles, review articles, and guidelines published in the past 5 years in peer-reviewed journals were first summarized. The original articles cited were then reviewed and relevant results were extracted.

Results

Patients with FPIES and non-IgE–mediated food allergic diseases developed vomiting, diarrhea, and food aversion expelled food allergen from their bodies. Aside from T helper type 2 (T_H2) immunity, T_H1, T_H17, innate immunity, and epithelial mucosal barrier defect were also found to be important in the pathogenesis. Eosinophils, widely identified in the biopsy samples, were key players or were late-recruited cells for tissue repairs in those diseases. Intestinal dysbiosis and their metabolites stimulated enterochromaffin cells or enteroendocrine cells to produce serotonin, interfering with intestinal motility and subsequently affecting brain function. FPIES and non-IgE–mediated food allergic diseases were likely part of the atopic march. Allergic inflammation in intestinal mucosa might result in subsequent inflammation in the airway mucosa, suggesting the theory of “one mucosa, one disease.”

Conclusion

The immune responses of FPIES and non-IgE–mediated food allergic diseases were not limited to the gastrointestinal tract, but also trigger wider inflammatory responses beyond it. Further research will be required to determine the systemic effect and intestinal microbiome of those diseases.

中文翻译：

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食物蛋白诱发的小肠结肠炎综合征和其他非免疫球蛋白E介导的食物过敏性疾病的胃肠道免疫病理学

客观的

为了简要概述有关食物蛋白诱发的小肠结肠炎综合征（FPIES）和其他非免疫球蛋白E（IgE）介导的食物过敏性疾病的胃肠道免疫病理学的最新文献。

数据源

数据是从PubMed，MEDLINE和ScienceDirect数据库中提取的。

研究选择

首先总结了过去5年间在同行评审期刊上发表的原始文章，评论文章和指南。然后对引用的原始文章进行审查，并提取相关结果。

结果

患有FPIES和非IgE介导的食物过敏性疾病的患者出现呕吐，腹泻，并且食物反感将食物过敏原从体内排出。除了2型T辅助（T _H 2）免疫力之外，T _H 1，T _H17，先天免疫和上皮粘膜屏障缺陷也被发现在发病机理中很重要。在活检样本中广泛鉴定到的嗜酸性粒细胞是这些疾病中组织修复的关键参与者或后期募集的细胞。肠道营养不良及其代谢产物刺激肠嗜铬细胞或肠内分泌细胞产生5-羟色胺，干扰肠蠕动并随后影响脑功能。FPIES和非IgE介导的食物过敏性疾病很可能是特应性行军的一部分。肠粘膜的过敏性炎症可能导致气道粘膜随后发生炎症，这提示了“一种粘膜，一种疾病”的理论。

结论

FPIES和非IgE介导的食物过敏性疾病的免疫反应不仅限于胃肠道，还可以引发更广泛的炎症反应。需要进一步的研究以确定这些疾病的全身作用和肠道微生物组。