title: Genetic variation in exon 10 of the BPI gene is associated with Escherichia coli F18 susceptibility in Sutai piglets.
abstract: Our aim was to investigate the effect of the porcine bactericidal/permeability-increasing protein (BPI) on the susceptibility to enterotoxigenic Escherichia coli F18 (ETEC F18). Specifically, we wanted to determine whether the HpaII restriction polymorphism in exon 10 of BPI mediates susceptibility to ETEC F18. Thirty verified ETEC F18-resistant and thirty susceptible Sutai (Duroc×Taihu) piglets were identified using the receptor binding assay. Exon 10 of the BPI gene produced the AA, BB, and AB genotypes after HpaII digestion. The genotype distribution among ETEC F18-resistant piglets was significantly different from that among susceptible piglets. Among piglets with the AA genotype, 90% were ETEC F18-resistant; this percentage of resistant piglets was significantly higher than the percentage of resistant piglets with the AB (57.1%) and BB genotypes (17.4%). There was high expression only in the tissues of the duodenum and jejunum, wherein the expression levels in the ETEC F18-resistant group were significantly higher than those in the susceptible group (P<0.05). The average expression levels in individuals with the AA genotype were significantly higher than those in individuals with the AB or BB genotype (P<0.05), while the results of Western blot show the same evidences as real time PCR. These results indicate that the upregulation of porcine BPI gene expression in the small intestines plays a direct role in resistance to ETEC F18 infection. The AA genotype for the HpaII site in exon 10 of the porcine BPI gene was demonstrated to be an anti-ETEC F18 marker and could be used for selective breeding to enhance ETEC F18 resistance.
authors.affiliation: Key Laboratory for Animal Genetics, Department of Animal Genetics, College of Animal Science and Technology, Yangzhou University, Yangzhou, Jiangsu, PR China.
authors.forename: Lu
authors.initials: L
authors.lastname: Liu
authors.forename: Jing
authors.initials: J
authors.lastname: Wang
authors.forename: Qiaohui
authors.initials: Q
authors.lastname: Zhao
authors.forename: Chen
authors.initials: C
authors.lastname: Zi
authors.forename: Zhengchang
authors.initials: Z
authors.lastname: Wu
authors.forename: Xianmin
authors.initials: X
authors.lastname: Su
authors.forename: Yongjiu
authors.initials: Y
authors.lastname: Huo
authors.forename: Guoqiang
authors.initials: G
authors.lastname: Zhu
authors.forename: Shenglong
authors.initials: S
authors.lastname: Wu
authors.forename: Wenbin
authors.initials: W
authors.lastname: Bao
mesh_terms: D000818:Animals; D023181:Antimicrobial Cationic Peptides / Q000235:genetics* / Q000378:metabolism; D001798:Blood Proteins / Q000235:genetics* / Q000378:metabolism; D015153:Blotting, Western; D060467:Disease Resistance / Q000235:genetics; D004386:Duodenum / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D004591:Electrophoresis, Polyacrylamide Gel; D054307:Enterotoxigenic Escherichia coli / Q000472:pathogenicity*; D004927:Escherichia coli Infections / Q000235:genetics / Q000382:microbiology / Q000662:veterinary*; D005091:Exons; D005786:Gene Expression Regulation; D014644:Genetic Variation; D005838:Genotype; D007583:Jejunum / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D017354:Point Mutation; D016133:Polymerase Chain Reaction / Q000379:methods; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D013552:Swine / Q000235:genetics* / Q000382:microbiology; D013553:Swine Diseases / Q000235:genetics / Q000382:microbiology
chemical_list: D023181:Antimicrobial Cationic Peptides; D001798:Blood Proteins; C021623:bactericidal permeability increasing protein