To test this hypothesis, we monoassociated IBD-susceptible 129SvEv IL10–/– and IBD-resistant IL10+/+ mice with AIEC CUMT8 (WT; B1, lpfA+, pduC+) (18), a strain that induces inflammation and Th17 responses in IL10–/– mice (14, 15); clusters with AIEC CU541-1 by genotype (19) and phenotype (Figures 3, 5, and 6); and parental derivatives of AIEC CUMT8 with engineered deletions in fucA (ΔfucA), pduC (ΔpduC), and eutH (ΔeutH) (15, 19) (Supplemental Figure 8, D–H). The gene discussed is FUCA1; the disease is inflammatory bowel disease.