Gliadin p31-43 (100?μg/mL; 30 minutes-6 hours) treatment induces the MyD88/TLR7 complexes, and activates downstream signalling by activating MAPKs, ERK, JNK and p38). Gliadin p31-43 increases the levels of the phosphorylated forms of pY-ERK, JNK (pY-JNK) and p38 (pY-p38)[1]. Gliadin p31-43 treatment increases NF-κB phosphorylation in CaCo-2 cells from 0.45?in control cells to 0.86. Gliadin p31-43 treatment induces a significant increase in levels of the MxA protein. The levels of the IFN-α 7 and 17 mRNAs are also analysed after Gliadin p31-43 treatment[1]. In CaCo-2 cells, Gliadin p31-43 localizes to the early endosomes and delays vesicular trafficking. Gliadin p31-43 interferes with the correct localization of the growth factor regulated tyrosine kinase substrate (HRS) to early endosomes, delaying the maturation of the endocytic vesicles[1]. Western Blot Analysis[1]Cell Line: CaCo-2 cells Concentration: 100?μg/mL Incubation Time: 30 minutes, 3 hours, 6 hours Result: Showed the increase in formation of the MyD88/TLR7 complex, and increased in the level of TLR7.

Gliadin p31-43 (10 μg; intraluminally injection) shows a sequence-specific spontaneous ability to form structured oligomers and aggregates in vitro and induced activation of the apoptosis-associated speck-like (ASC) complex[2]. The increment of IL-1β indicates the activation of the inflammasome caspase-1 pathway in the small intestine mucosa by oral administration of Gliadin p31-43 (20 μg) in wild type C57Bl/6 mice. Gliadin p31-43 has an intrinsic propensity to form oligomers which trigger the NLRP3 inflammasome[2].