Departamento de Ciencias Biológicas, Facultad de Ciencias Exactas, Instituto de Estudios Inmunológicos y Fisiopatológicos-IIFP (UNLP-CONICET), La Plata, Argentina.
European Laboratory for the Investigation of Food Induced Diseases (ELFID), University Federico II, Naples, Italy.
Int Rev Cell Mol Biol. 2021;358:165-205. doi: 10.1016/bs.ircmb.2020.10.003. Epub 2020 Nov 5.
Coeliac disease (CD) is the prototype of an inflammatory chronic disease induced by food. In this context, gliadin p31-43 peptide comes into the spotlight as an important player of the inflammatory/innate immune response to gliadin in CD. The p31-43 peptide is part of the p31-55 peptide from α-gliadins that remains undigested for a long time, and can be present in the small intestine after ingestion of a gluten-containing diet. Different biophysical methods and molecular dynamic simulations have shown that p31-43 spontaneously forms oligomeric nanostructures, whereas experimental approaches using in vitro assays, mouse models, and human duodenal tissues have shown that p31-43 is able to induce different forms of cellular stress by driving multiple inflammatory pathways. Increased proliferative activity of the epithelial cells in the crypts, enterocyte stress, activation of TG2, induction of Ca, IL-15, and NFκB signaling, inhibition of CFTR, alteration of vesicular trafficking, and activation of the inflammasome platform are some of the biological effects of p31-43, which, in the presence of appropriate genetic susceptibility and environmental factors, may act together to drive CD.
乳糜泻（CD）是由食物引起的炎症性慢性疾病的典型范例。在这种情况下，麦醇溶蛋白 p31-43 肽成为麦醇溶蛋白中诱导炎症/先天免疫反应的重要参与者。p31-43 肽是来自 α-麦醇溶蛋白的 p31-55 肽的一部分，该肽在很长一段时间内未被消化，并可在摄入含麸质饮食后存在于小肠中。不同的生物物理方法和分子动力学模拟表明，p31-43 会自发形成寡聚纳米结构，而使用体外测定、小鼠模型和人十二指肠组织的实验方法表明，p31-43 通过驱动多种炎症途径诱导不同形式的细胞应激。隐窝中上皮细胞的增殖活性增加、肠细胞应激、TG2 的激活、Ca、IL-15 和 NFκB 信号的诱导、CFTR 的抑制、囊泡运输的改变以及炎症小体平台的激活是 p31-43 的一些生物学效应，这些效应在适当的遗传易感性和环境因素的存在下，可能共同作用导致 CD。
