title: Effect of susceptibility to enterotoxigenic Escherichia coli F4 and of dietary tryptophan on gut microbiota diversity observed in healthy young pigs.
abstract: Healthy weaned pigs susceptible to enterotoxigenic Escherichia coli F4 (ETEC) require more tryptophan (Trp) to maximize their performance. This may be related to an effect on intestinal microbiota. We studied the intestinal bacterial diversity of healthy pigs with different susceptibility to ETEC and fed different Trp levels. Thirty-six littermate weaned pigs were selected to obtain a set potentially formed of 50% ETEC-susceptible and 50% non-susceptible pigs, based on a Mucin 4 gene polymorphism. Pigs were fed a diet with 0.17 (TrpL) or 0.22 (TrpH) standardized ileal digestible Trp:Lys ratio for 21 days. Slaughtered pigs were classified into non-susceptible, mildly susceptible, and susceptible, by testing ETEC adhesion to intestinal villi. Bacterial diversity in jejunum content was assessed by the 16S rRNA gene-targeted denaturing gradient gel electrophoresis (DGGE) fingerprinting analysis and expressed by the Shannon index. Susceptible pigs had a reduced bacterial diversity, particularly with TrpL diet (p=0.003). The ETEC adhesion class affected the quantification of enterobacteria DNA (p=0.027). One DGGE band, which referred to Clostridium bartlettii, was not evidenced in all the susceptible pigs; less DNA from this microbe was quantified by RT-PCR in the jejunum from TrpH susceptible pigs (p=0.025) compared to TrpL. The gene expression for β-galactoside α-2,3-sialyltransferase 1 was higher in jejunal tissue of ETEC-susceptible pigs (p=0.019). In studies on pig gut microbiota, the presence of intestinal receptors for ETEC should be considered because of their contribution to a reduced bacterial diversity. This effect could be partially reversed by dietary Trp addition.
authors.affiliation: University of Bologna, Diproval, Via Rosselli 107, 42123 Reggio Emilia, Italy.
authors.forename: Stefano
authors.initials: S
authors.lastname: Messori
authors.forename: Paolo
authors.initials: P
authors.lastname: Trevisi
authors.forename: Aude
authors.initials: A
authors.lastname: Simongiovanni
authors.forename: Davide
authors.initials: D
authors.lastname: Priori
authors.forename: Paolo
authors.initials: P
authors.lastname: Bosi
mesh_terms: D000818:Animals; D001422:Bacterial Adhesion; D058645:Denaturing Gradient Gel Electrophoresis; D004032:Diet; D004198:Disease Susceptibility; D054307:Enterotoxigenic Escherichia coli / Q000472:pathogenicity*; D004927:Escherichia coli Infections / Q000235:genetics / Q000378:metabolism / Q000382:microbiology / Q000662:veterinary*; D005260:Female; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000382:microbiology*; D007583:Jejunum / Q000378:metabolism / Q000382:microbiology; D008297:Male; D064307:Microbiota; D055264:Mucin-4 / Q000235:genetics; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D012799:Sialyltransferases / Q000235:genetics; D034421:Sus scrofa; D013552:Swine; D013553:Swine Diseases / Q000235:genetics / Q000378:metabolism / Q000382:microbiology*; D014364:Tryptophan / Q000008:administration & dosage* / Q000378:metabolism; D014886:Weaning; D000094663:beta-Galactoside alpha-2,3-Sialyltransferase
chemical_list: D055264:Mucin-4; D012336:RNA, Ribosomal, 16S; D014364:Tryptophan; D012799:Sialyltransferases; D000094663:beta-Galactoside alpha-2,3-Sialyltransferase