Abstract
BackgroundBurkholderia pseudomallei and Burkholderia mallei cause the diseases melioidosis and glanders, respectively. A well-studied aspect of pathogenesis by these closely-related bacteria is their ability to invade and multiply within eukaryotic cells. In contrast, the means by which B. pseudomallei and B. mallei adhere to cells are poorly defined. The purpose of this study was to identify adherence factors expressed by these organisms.ResultsComparative sequence analyses identified a gene product in the published genome of B. mallei strain ATCC23344 (locus # BMAA0649) that resembles the well-characterized Yersinia enterocolitica autotransporter adhesin YadA. The gene encoding this B. mallei protein, designated boaA, was expressed in Escherichia coli and shown to significantly increase adherence to human epithelial cell lines, specifically HEp2 (laryngeal cells) and A549 (type II pneumocytes), as well as to cultures of normal human bronchial epithelium (NHBE). Consistent with these findings, disruption of the boaA gene in B. mallei ATCC23344 reduced adherence to all three cell types by ~50%. The genomes of the B. pseudomallei strains K96243 and DD503 were also found to contain boaA and inactivation of the gene in DD503 considerably decreased binding to monolayers of HEp2 and A549 cells and to NHBE cultures.A second YadA-like gene product highly similar to BoaA (65% identity) was identified in the published genomic sequence of B. pseudomallei strain K96243 (locus # BPSL1705). The gene specifying this protein, termed boaB, appears to be B. pseudomallei-specific. Quantitative attachment assays demonstrated that recombinant E. coli expressing BoaB displayed greater binding to A549 pneumocytes, HEp2 cells and NHBE cultures. Moreover, a boaB mutant of B. pseudomallei DD503 showed decreased adherence to these respiratory cells. Additionally, a B. pseudomallei strain lacking expression of both boaA and boaB was impaired in its ability to thrive inside J774A.1 murine macrophages, suggesting a possible role for these proteins in survival within professional phagocytic cells.ConclusionsThe boaA and boaB genes specify adhesins that mediate adherence to epithelial cells of the human respiratory tract. The boaA gene product is shared by B. pseudomallei and B. mallei whereas BoaB appears to be a B. pseudomallei-specific adherence factor.
Highlights
Burkholderia pseudomallei and Burkholderia mallei cause the diseases melioidosis and glanders, respectively
The present study reports the identification of B. pseudomallei and B. mallei gene products that mediate adherence to epithelial cells derived from the human respiratory tract, relevant to the aerosol route of infection by these organisms
Identification of a gene shared by B. mallei and B. pseudomallei that encodes a potential autotransporter adhesin Analysis of the annotated genomic sequence of B. mallei ATCC23344 identified the open reading frame (ORF) locus tag number BMAA0649 as resembling members of the oligomeric coiled-coil adhesin (Oca) family of autotransporter proteins [55]
Summary
Burkholderia pseudomallei and Burkholderia mallei cause the diseases melioidosis and glanders, respectively. B. mallei ATCC23344 was found to specify a large number of mobile DNA elements that have contributed to extensive deletions and rearrangements relative to the genome of B. pseudomallei K96243. Despite these differences, the genes shared by the two isolates have an average identity of 99% at the nucleotide level [19,26]. B. pseudomallei causes the human disease melioidosis, which is notoriously difficult to diagnose. Infection occurs via inhalation of contaminated aerosol particles or through skin abrasions, and the risk of contracting the disease is proportional to the concentration of B. pseudomallei in soil and water. Response to treatment is slow and eradication of B. pseudomallei is difficult to achieve, resulting in recrudescence [1,37,38,39]
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