Cornell H J, Auricchio R S, De Ritis G, De Vincenzi M, Maiuri L, Raia V, Silano V
Department of Applied Chemistry, Royal Melbourne Institute of Technology, Melbourne, Australia.
Pediatr Res. 1988 Aug;24(2):233-7. doi: 10.1203/00006450-198808000-00019.
Subfraction 2R of fraction 9 from a peptic-tryptic-pancreatic digest of wheat gliadin is known to be toxic in vivo to celiac patients. We have found that fractions 9 and 2R inhibit the in vitro development of fetal rat intestine and the increase of enterocyte height occurring in organ culture of atrophic celiac mucosa (0.1-0.5 mg/ml medium). Other peptide fractions of the gliadin digest are devoid of such in vitro effects. Subfraction 2R, after incubation with morphologically normal small intestinal mucosa of celiacs in remission and ultrafiltration, was still very active in both culture systems at low concentration (0.1 mg/ml); on the contrary, subfraction 2R was inactivated after incubation with normal mucosa. These results are compatible with the hypothesis that there is a mucosal defect in handling gliadin peptides in celiac disease, and suggest that there is either a primary (or secondary) enzyme deficiency or some other mechanism operating in the intestinal mucosa of celiac patients in remission.
已知从小麦醇溶蛋白的胃蛋白酶 - 胰蛋白酶 - 胰酶消化物的第9部分中得到的2R亚组分在体内对乳糜泻患者有毒性。我们发现第9部分和2R亚组分在体外会抑制胎鼠肠道的发育以及萎缩性乳糜泻黏膜器官培养中肠上皮细胞高度的增加(培养基中浓度为0.1 - 0.5毫克/毫升)。醇溶蛋白消化物的其他肽组分没有这种体外效应。2R亚组分在与处于缓解期的乳糜泻患者形态正常的小肠黏膜一起孵育并超滤后,在两种培养系统中低浓度(0.1毫克/毫升)时仍具有很高活性;相反,2R亚组分与正常黏膜孵育后会失活。这些结果与以下假设相符,即乳糜泻中在处理醇溶蛋白肽方面存在黏膜缺陷,并表明在处于缓解期的乳糜泻患者的肠黏膜中存在原发性(或继发性)酶缺乏或其他一些作用机制。