Up to 20% of people worldwide develop gastrointestinal symptoms following a meal¹, leading to decreased quality of life, substantial morbidity and high medical costs. Although the interest of both the scientific and lay communities in this issue has increased markedly in recent years, with the worldwide introduction of gluten-free and other diets, the underlying mechanisms of food-induced abdominal complaints remain largely unknown. Here we show that a bacterial infection and bacterial toxins can trigger an immune response that leads to the production of dietary-antigen-specific IgE antibodies in mice, which are limited to the intestine. Following subsequent oral ingestion of the respective dietary antigen, an IgE- and mast-cell-dependent mechanism induced increased visceral pain. This aberrant pain signalling resulted from histamine receptor H₁-mediated sensitization of visceral afferents. Moreover, injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with irritable bowel syndrome induced local oedema and mast cell activation. Our results identify and characterize a peripheral mechanism that underlies food-induced abdominal pain, thereby creating new possibilities for the treatment of irritable bowel syndrome and related abdominal pain disorders.

全球多达 20% 的人在饭后出现胃肠道症状¹，导致生活质量下降、发病率高和医疗费用高。尽管近年来科学界和非专业人士对此问题的兴趣显着增加，但随着全球无麸质和其他饮食的引入，食物引起的腹部不适的潜在机制仍然很大程度上未知。在这里，我们表明细菌感染和细菌毒素可以触发免疫反应，导致小鼠产生饮食抗原特异性 IgE 抗体，这些抗体仅限于肠道。随后口服摄入相应的膳食抗原后，IgE 和肥大细胞依赖性机制诱导内脏疼痛增加。这种异常的疼痛信号是由组胺受体 H _1引起的-介导的内脏传入敏感。此外，将食物抗原（麸质、小麦、大豆和牛奶）注射到肠易激综合征患者的直肠乙状结肠粘膜中会引起局部水肿和肥大细胞活化。我们的研究结果确定并表征了食物引起的腹痛的外围机制，从而为治疗肠易激综合征和相关腹痛疾病创造了新的可能性。