In all three models, acute Citrobacter rodentium infection in the colon, chronic Helicobacter pylori infection in the stomach, and DSS-induced colitis, A-Eos were increased compared to B-Eos and demonstrated upregulation of genes involved in granulogenesis, antimicrobial activity, immune modulation, IFNɣ signaling, and major histocompatibility complex class I (MHC-1)-restricted antigen processing and presentation. This evidence concerns the gene IFNA1 and colitis.