ArticleJournal of animal science2026
FUT1 genetic polymorphism influences susceptibility to F18 enterotoxigenic Escherichia coli infection in pigs.
Article in Journal of animal science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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