Wheat Amylase Trypsin Inhibitors Aggravate Intestinal Inflammation Associated with Celiac Disease Mediated by Gliadin in BALB/c Mice
文献类型： 外文期刊
作者： Yu, Tian 1 ; Hu, Shuai 4 ; Min, Fangfang 1 ; Li, Jingjing 1 ; Shen, Yunpeng 1 ; Yuan, Juanli 1 ; Gao, Jinyan 3 ; Wu, Yong 1 ; Chen, Hongbing 1 ;
作者机构： 1.Nanchang Univ, State Key Lab Food Sci & Technol, Nanchang 330047, Jiangxi, Peoples R China
2.Nanchang Univ, Sino German Joint Res Inst, Nanchang 330047, Jiangxi, Peoples R China
3.Nanchang Univ, Sch Food Sci & Technol, Nanchang 330031, Jiangxi, Peoples R China
4.Jiangxi Acad Agr Sci, Inst Agr Prod Proc, Nanchang 330200, Jiangxi, Peoples R China
5.Nanchang Univ, Sch Pharmaceut Sci, Nanchang 330006, Jiangxi, Peoples R China
关键词： wheat amylase trypsin inhibitors; celiac disease; gliadin; intestinal inflammation; Th1/Th2
期刊名称：FOODS （ 影响因子：5.561； 五年影响因子：5.94 ）
ISSN：
年卷期： 2022 年 11 卷 11 期
页码：
收录情况： SCI
摘要： Celiac disease (CD) is an autoimmune intestinal disorder caused by the ingestion of gluten in people who carry the susceptible gene. In current celiac disease research, wheat gluten is often the main target of attention, neglecting the role played by non-gluten proteins. This study aimed to describe the effects of wheat amylase trypsin inhibitors (ATI, non-gluten proteins) and gliadin in BALB/c mice while exploring the further role of relevant adjuvants (cholera toxin, polyinosinic: polycytidylic acid and dextran sulfate sodium) intervention. An ex vivo splenocyte and intestinal tissue were collected for analysis of the inflammatory profile. The consumption of gliadin and ATI caused intestinal inflammation in mice. Moreover, the histopathology staining of four intestinal sections (duodenum, jejunum, terminal ileum, and middle colon) indicated that adjuvants, especially polyinosinic: polycytidylic acid, enhanced the villi damage and crypt hyperplasia in co-stimulation with ATI and gliadin murine model. Immunohistochemical results showed that tissue transglutaminase and IL-15 expression were significantly increased in the jejunal tissue of mice treated with ATI and gliadin. Similarly, the expression of inflammatory factors (TNF-alpha, IL-1 beta, IL-4, IL-13) and Th1/Th2 balance also showed that the inflammation response was significantly increased after co-stimulation with ATI and gliadin. This study provided new evidence for the role of wheat amylase trypsin inhibitors in the pathogenesis of celiac disease.
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