Highly expressed genes in a rough-colony-forming phenotype of Aggregatibacter actinomycetemcomitans: implication of a mip-like gene for the invasion of host tissue

FEMS Immunol Med Microbiol. 2010 Mar;58(2):226-36. doi: 10.1111/j.1574-695X.2009.00624.x. Epub 2009 Nov 20.

Abstract

Aggregatibacter actinomycetemcomitans, a potent pathogen of periodontitis, typically grows as a rough and adherent colony on primary isolated cultures. The colony transforms into a smooth phenotype during repeated subculture. In this study, we aimed to identify highly expressed genes in the rough-colony-forming phenotype for isolation of host-induced genes. Using a cDNA-subtractive hybridization technique, three genes, homologous to a macrophage infectivity potentiator gene (mip), peroxiredoxin gene (prx) and outer membrane protein gene (ompA), were identified. The expression levels of these genes in the rough-colony-forming phenotype were 4-10-fold higher as compared with the smooth-colony-forming phenotype. Attention was focused on the mip-like gene, and a recombinant protein and a deficient mutant were constructed. The recombinant protein reacted with sera from patients with periodontitis, suggesting the production of the Mip-like protein in periodontal lesions. Viable quantitative invasion assay demonstrated that the viable cell counts of the wild-type strain that invaded HeLa cells were more than fourfold as compared with the mip-deficient mutant. The expression of the mip-like gene, prx-like gene and ompA-like gene may be enhanced in the host, and the mip-like gene may play an important role in the infection of A. actinomycetemcomitans, especially in its invasion of the epithelium.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antibodies, Bacterial / blood
  • Bacterial Proteins / biosynthesis*
  • Bacterial Proteins / genetics
  • Colony Count, Microbial
  • Epithelial Cells / microbiology
  • Gene Deletion
  • Gene Expression Regulation, Bacterial*
  • HeLa Cells
  • Humans
  • Nucleic Acid Hybridization
  • Pasteurellaceae / genetics*
  • Pasteurellaceae / pathogenicity*
  • Periodontitis / immunology
  • Recombinant Proteins / genetics
  • Recombinant Proteins / immunology
  • Virulence
  • Virulence Factors / biosynthesis*
  • Virulence Factors / deficiency

Substances

  • Antibodies, Bacterial
  • Bacterial Proteins
  • Recombinant Proteins
  • Virulence Factors
  • Mip-like protein, Chlamydia trachomatis