Article

IbeB is involved in the invasion and pathogenicity of avian pathogenic Escherichia coli.

Key Lab of Animal Bacteriology, Ministry of Agriculture, Nanjing Agricultural University, Nanjing 210095, China.
Veterinary Microbiology (Impact Factor: 3.13). 04/2012; 159(3-4):411-9. DOI: 10.1016/j.vetmic.2012.04.015
Source: PubMed

ABSTRACT The ibeB gene in neonatal meningitis Escherichia coli (NMEC) contribute to the penetration of human brain microvascular endothelial cells (HBMECs). However, whether IbeB plays a role in avian pathogenic E. coli (APEC) infection remains unclear. Thus, this study was conducted to investigate the distribution of the ibeB gene in Chinese APEC strains and examine whether IbeB is involved in APEC pathogenicity. The ibeB gene was found in all 100 detected E. coli isolates with over 97% sequence homology. These results indicated that ibeB is a conserved E. coli gene irrelevant of pathotypes. To determine the role of ibeB in APEC pathogenicity, an ibeB mutant of strain DE205B was constructed and characterized. The inactivation of ibeB resulted in reduced invasion capacity towards DF-1 cells and defective virulence in animal models as compared to the wild-type strain. Animal infection experiments revealed that loss of ibeB decreased APEC colonization and invasion capacity in brains and lungs. These virulence-related phenotypes were partially recoverable by genetic complementation. Reduced expression levels of invasion- and adhesion-associated genes in ibeB mutant could be major reasons as evidenced by reduced ibeA and ompA expression. These results indicate that IbeB is involved in APEC invasion and pathogenicity.

0 Bookmarks
 · 
147 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Avian pathogenic Escherichia coli (APEC) cause respiratory and systemic disease in poultry. Sequencing of a multi-locus sequence type (ST)-95 serogroup O1 strain previously indicated that APEC resemble E. coli causing human extra-intestinal diseases. We sequenced the genomes of two strains of another dominant APEC lineage (ST23 serogroup O78 strains χ7122 and IMT2125) and compared them to each other and the reannotated APEC O1 sequence. For comparison, we also sequenced a human enterotoxigenic E. coli (ETEC) strain of the same ST23 serogroup O78 lineage. Phylogenetic analysis indicated that the APEC O78 strains were more closely related to a human ST23 ETEC than APEC O1, indicating that separation of pathotypes on the basis of being extra-intestinal or diarrheagenic is not supported by their phylogeny. The accessory genome of APEC ST23 strains exhibited limited conservation of APEC O1 genomic islands and a distinct repertoire of virulence-associated loci. In light of this diversity, we surveyed the phenotype of 2185 χ7122 signature-tagged transposon mutants following intra-air sac inoculation of turkeys. This identified novel APEC ST23 genes that play strain- and tissue-specific roles during infection. For example, genes mediating group 4 capsule synthesis were required for virulence of χ7122 and conserved in IMT2125 but absent from APEC O1. Our data reveal the genetic diversity of E. coli adapted to cause the same avian disease and indicate that the core genome of the ST23 lineage serves as a chassis for evolution of E. coli adapted to cause avian or human disease via acquisition of distinct virulence genes.
    Infection and immunity 12/2012; · 4.21 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Macrophages are immune cells that are known to engulf pathogens and destroy them by employing several mechanisms, including oxidative burst, induction of Fe(II) and Mn(II) efflux, and through elevation of Cu(I) and Zn(II) concentrations in the phagosome ('brass dagger'). The importance of the latter mechanism is supported by the presence of multiple counteracting efflux systems in bacteria, responsible for the efflux of toxic metals. We hypothesize that similar bacteria-killing mechanisms are found in predatory protozoa/amoeba species. Here, we present a brief summary of soft metal-related mechanisms used by macrophages, and perhaps amoeba, to inactivate and destroy bacteria. Based on this, we think it is likely that copper resistance is also selected for by protozoan grazing in the environment.
    Future Microbiology 10/2013; 8:1257-64. · 4.02 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Autotransporter (AT) proteins constitute a large family of extracellular proteins that contribute to bacterial virulence. A novel AT adhesin gene aatB was identified in avian pathogenic E. coli (APEC) DE205B via genomic analyses. The open reading frame of aatB was 1017 bp, coding a putative 36.3 kDa protein, which contained structural motifs characteristic for AT proteins: a signal peptide, a passenger domain, and a translocator domain. The predicted three-dimensional structure of AatB consisted of two distinct domains, the C-terminal β-barrel translocator domain and an N-terminal passenger domain. The prevalence analyses of aatB in APEC indicated that aatB was detected in 26.4% (72/273) of APEC strains, which was strongly associated with phylogenetic groups D and B2. Quantitative real-time reverse transcription-PCR analyses revealed that AatB expression was increased during infection in vitro and in vivo. Moreover, AatB could elicit antibodies in infected ducks, suggesting AatB was involved in APEC pathogenicity. Thus, mutant and complement strains of aatB gene in APEC DE205B were constructed. Inactivation of aatB resulted in the reduced capacity to adhere to DF-1 cells, defective virulence in vivo, and decreased colonization capacity in lung during the systemic infection compared with wild-type strain. Furthermore, these capacities were restored in the complementation strains. These results indicated that AatB makes a significant contribution to APEC virulence through bacterial adherence to host tissues in vivo and in vitro. In addition, biofilm formation assays for strain AAEC189 expressing AatB indicated that AatB mediates biofilm formation.
    Infection and immunity 04/2013; · 4.21 Impact Factor