Profiling inflammatory outcomes of colonization and food allergy induction in the murine glandular stomach.

UNLABELLED

We investigated the effects of colonization on inflammatory responses in the murine glandular stomach, which is similar to the glandular mucosa of the human stomach. We also explored whether the presence of a food allergy could exacerbate -induced inflammation or if would amplify allergic inflammation in the glandular stomach. successfully colonized the stomach of amoxicillin-pre-treated BALB/c mice and induced gastritis in the limiting ridge with minimal inflammation in the glandular stomach. There was significant upregulation of , calprotectin ( and ), and several antimicrobial peptides, but minimal induction of type 1, 2, or 3 responses in the glandular stomach. A robust type 2 response, inflammatory cell recruitment, and tissue remodeling occurred in the glandular stomach following oral ovalbumin challenges in sensitized mice. The type 2 response was not augmented by colonization, but there was significant upregulation of , , , and in -colonized food allergic mice. The presence of did not affect the expression of genes involved in barrier integrity and signaling, many of which were upregulated during food allergy. Overall, our data indicate that colonization induces minimal inflammation in the glandular stomach but augments antimicrobial peptide expression. Induction of a food allergy results in robust type 2 inflammation in the glandular stomach, and while colonization does not exacerbate type 2 inflammation, it does activate a number of innate and type 3 immune responses amid the backdrop of allergic inflammation.

IMPORTANCE

Food allergy continues to be a growing public health concern, affecting at least 1 in 10 individuals in the United States alone. However, little is known about the involvement of the gastric mucosa in food allergy. Gastrointestinal colonization has been reported to promote gastrointestinal inflammation in a number of chronic diseases. Using a mouse model of food allergy to egg white protein, we demonstrate regionalization of the inflammatory response to colonization, induction of robust type 2 (allergic) inflammation in the stomach, and augmentation of innate and type 3 responses by colonization during food allergy.