Due to the worldwide epidemic of allergic disease and a cure nowhere in sight, there is a crucial need to explore its pathophysiological mechanisms. As allergic disease has been associated with gut dysbiosis, we searched for a possible mechanism from the perspective of the molecular interface between host and microbiota with concurrent metabolomics and microbiome composition analysis. Sprague-Dawley rats were injected with Artemisia pollen extract to stimulate a hyper reaction to pollen. This hyper reaction decreased the circulation of valine, isoleucine, aspartate, glutamate, glutamine, indole-propionate (IPA), and myo-inositol, and reduced short-chain fatty acids (SCFAs) in feces. Several beneficial genera belonging to Ruminococcaceae, Lachnospiraceae, and Clostridiales declined in the model group, whereas Helicobacter and Akkermansia were only expressed in the model group. Furthermore, the expression of intestinal claudin-3 and liver fatty acid binding protein was downregulated in the model group and associated with metabolic changes and bacteria. Our results suggest that alterations in amino acids as well as their derivatives (especially valine, and IPA which is the reductive product of tryptophan), SCFAs, and the gut microbiome (specifically Akkermansia and Helicobacter) may disrupt the intestinal barrier function by inhibiting the expression of claudin proteins and affecting the mucus layer, which further results in hay fever.

由于过敏性疾病在全球范围内流行，且治愈方法遥遥无期，因此迫切需要探索其病理生理机制。由于过敏性疾病与肠道菌群失调有关，我们从宿主和微生物群之间的分子界面的角度寻找可能的机制，同时进行代谢组学和微生物组组成分析。Sprague-Dawley 大鼠被注射艾蒿花粉提取物以刺激对花粉的过度反应。这种过度反应减少了缬氨酸、异亮氨酸、天冬氨酸、谷氨酸、谷氨酰胺、吲哚丙酸 (IPA) 和肌醇的循环，并减少了粪便中的短链脂肪酸 (SCFA)。属于瘤胃球菌科、毛螺菌科和梭菌目的几个有益属在模型组中下降，而螺杆菌和阿克曼氏菌仅在模型组中表达。此外，模型组肠道claudin-3和肝脏脂肪酸结合蛋白的表达下调，并与代谢变化和细菌有关。我们的研究结果表明，氨基酸及其衍生物（尤其是缬氨酸和 IPA，它是色氨酸的还原产物）、SCFA 和肠道微生物组（特别是Akkermansia和螺杆菌）的改变可能通过抑制表达来破坏肠道屏障功能密蛋白和影响粘液层，这进一步导致花粉热。