aEPEC have a highly diverse virulence factor and effector protein repertoire due to evolution via repeated acquisition of LEE PAI variants and overall genetic plasticity.24 It has been previously suggested that differences in the effector protein arsenal could explain the heterogeneous clinical phenotypes of aEPEC infection.25,26,51 We showed that aEPEC from UC patients elicited a stronger epithelial IL-8 response than aEPEC from CD, which behaved more like tEPEC. This evidence concerns the gene CXCL8 and infection.