Food allergies can cause intestinal damage that can exacerbate allergic symptoms, and gut microbiota have been shown to influence allergic development. This study was intended to investigate the effects of Avenanthramide (AVA) on colonic damage induced by food allergy and its mechanism. In Exp. 1, AVA administrations alleviated colonic inflammation in mice challenged with ovalbumin, as shown by decreased concentrations of TNF-α, IL-25 and IL-33. Additionally, the AVA supplementations improved intestinal barrier damage by elevating occludin, ZO-1 and claudin-1 levels. Moreover, AVA inhibited NF-κB phosphorylation and enhanced heat shock protein 70 (Hsp70) expression in the colon. In Exp. 2, apoptozole as a Hsp70 inhibitor was used to explore the Hsp70-NF-κB signaling contribution to AVA function. The AVA additions increased the productions of acetate and butyrate, but decreased propionate. Notably, AVA reduced the colonic abundance of propionate-producing microbes such as Muribaculaceae, but elevated butyrate-producing microbes including Roseburia, Blautia, and Lachnospiraceae_NK4A136_group. Microbial alteration could be responsible for the increased butyrate, and thus the up-regulated Hsp70. However, apoptozole treatment eliminated the effects of AVA. Our study revealed that AVA improved colonic injury and inflammation induced by food allergies, and this mechanism may be mediated by the increased microbial-derived butyrate and involved in the Hsp70-NF-κB signaling.
Keywords: Hsp70-NF-κB signaling; avenanthramide; butyrate; colonic injury; food allergy; gut microbiota.