FUT1 genetic polymorphism influences susceptibility to F18 enterotoxigenic Escherichia coli infection in pigs.

F18 enterotoxigenic Escherichia coli (ETEC) causes post-weaning diarrhea in nursery pigs, with susceptibility determined by a polymorphism in the α(1,2)-fucosyltransferase (FUT1) gene at nucleotide M307, where FUT1-M307A/A pigs are deemed F18 resistant and FUT1-M307G/A and FUT1-M307G/G pigs are deemed F18 susceptible to bacterial attachment. This post hoc analysis evaluated the effect of FUT1 genotype on disease susceptibility following F18 ETEC challenge over 3 experiments. It was hypothesized that FUT1 susceptible pigs (G/G and G/A) would incur greater F18 attachment than FUT1 resistant pigs (A/A). In Exp. 1 and 2, 194 pigs (5.79 ± 1.02 kg BW; 12% FUT1-M307G/G, 52% FUT1-M307G/A, 36% FUT1-M307A/A) were allocated to pens (6 pigs/pen), and half were orally inoculated with ∼1 × 109 CFU/mL F18 ETEC on d 10 (d-post infection [dpi] 0). Individual pig body weights (BW) were recorded on dpi -10, 0, 5, 12, and 28 to calculate growth rates. In Exp. 3, 18 individually housed pigs (5.68 ± 0.51 kg BW; 6% FUT1-M307G/G, 65% FUT1-M307G/A, 29% FUT1-M307A/A) were inoculated on d 10 (dpi 0) with ∼1 × 107-109 CFU/mL and euthanized at dpi 5 for collection of ileal tissue and digesta to evaluate ileal F18 ETEC attachment, cystic fibrosis transmembrane conductance regulator (CFTR) abundance, and F18 gene abundance. From dpi 0 to 5, growth rates were reduced by 58.9% and 62.2% in FUT1-M307G/A and FUT1-M307G/G pigs, respectively, compared with unchallenged controls, whereas FUT1-M307A/A pigs growth rates were unaffected (P < 0.0001). Over the entire post-infection period (dpi 0-28), growth rate and mortality did not differ between genotypes or F18 ETEC challenge (P > 0.10). Ileal F18 attachment tended to be greatest in G/G pigs compared with G/A and A/A pigs (2.6%, 1.2%, 0.1, respectively; P < 0.10). Ileal CFTR abundance was greater in G/G relative to G/A and A/A pigs (3.1%, 1.1%, 0.3%, respectively; P < 0.05). Ileal F18 gene abundance tended to be highest in G/G pigs (21.7) compared with G/A (18.0) and A/A (12.7) pigs (P < 0.10). In conclusion, FUT1 genetic polymorphisms G/G and G/A can increase susceptibility to F18 ETEC infection, warranting further investigation into interactions with other intestinal microbes, and representing a promising target for genetic selection.