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-α, IL-1β, 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.