title: The luxS gene functions in the pathogenesis of avian pathogenic Escherichia coli.
abstract: Avian pathogenic Escherichia coli (APEC) causes avian colibacillosis, the most significant infectious bacterial disease of poultry worldwide. LuxS, the product of the luxS gene, mediates the quorum sensing (QS) mechanism. This involves the production of autoinducer-2 (AI-2), which regulates important physiological traits and a variety of adaptive processes in different bacteria. In this study, a luxS gene deleted APEC mutant strain, ΔDE17, was constructed using strain DE17. Analysis of bioluminescence indicated that deletion of the luxS gene abolished the production of the QS signal AI-2 in the bacteria. Further studies showed that deletion of the luxS gene in DE17 reduced the bacterial virulence by 31.5-fold in ducklings, based on the measurement of the 50% lethal dose. The mutant strain reduced significantly the abilities of adherence and invasion, by 50.0% and 40.7% respectively, compared with the wild strain DE17. The mutant strain also showed reduced survival in vivo: the bacterial loads of the mutant strain in infected liver, spleen and blood were 46.4-fold, 5.2-fold, and 3.7-fold reduced, respectively, compared with the wild-type strain DE17. Real-time polymerase chain reaction (PCR) demonstrated further that the mRNA levels of the virulence-related genes iucD, fyuA, vat, ompA, iss, fimC and tsh were significantly decreased in the mutant strain ΔDE17, when compared with DE17 (p < 0.05). In addition, the deletion of the luxS gene reduced the motility of the bacterium. This study suggests that the luxS gene functions in the pathogenesis of diseases caused by avian pathogenic E. coli.
authors.affiliation: Shanghai Veterinary Research Institute, The Chinese Academy of Agricultural Sciences, Shanghai, PR China.
authors.forename: Xiangan
authors.initials: X
authors.lastname: Han
authors.forename: Hao
authors.initials: H
authors.lastname: Bai
authors.forename: Lei
authors.initials: L
authors.lastname: Liu
authors.forename: Hongliang
authors.initials: H
authors.lastname: Dong
authors.forename: Rui
authors.initials: R
authors.lastname: Liu
authors.forename: Jun
authors.initials: J
authors.lastname: Song
authors.forename: Chan
authors.initials: C
authors.lastname: Ding
authors.forename: Kezong
authors.initials: K
authors.lastname: Qi
authors.forename: Haiwen
authors.initials: H
authors.lastname: Liu
authors.forename: Shengqing
authors.initials: S
authors.lastname: Yu
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D013437:Carbon-Sulfur Lyases / Q000235:genetics / Q000378:metabolism*; D004372:Ducks; D004926:Escherichia coli / Q000235:genetics / Q000472:pathogenicity* / Q000502:physiology*; D004927:Escherichia coli Infections / Q000382:microbiology / Q000662:veterinary*; D005260:Female; D015964:Gene Expression Regulation, Bacterial; D008297:Male; D011201:Poultry Diseases / Q000382:microbiology*; D053038:Quorum Sensing; D017384:Sequence Deletion; D014774:Virulence
chemical_list: D001426:Bacterial Proteins; D013437:Carbon-Sulfur Lyases; C117753:LuxS protein, Bacteria