ELAINE HAASE, PhD personal profile
The periodontal pathogen Actinobacillus actinomycetemcomitans (Aa) exhibits at least two phenotypes in vitro. Primary clinical isolates have a rough phenotype and form a very tenacious biofilm when grown in liquid culture. Upon continuous subculture, the organism undergoes irreversible phase transition to a minimally adhesive smooth phenotype.
Though the rough variant appears to be the virulent form of this organism, there may be a role for both the rough and smooth variants within the multiple microenvironments of the oral cavity that may occur during chronic infection. For example, the rough variant is able to persist on rat teeth whereas the smooth variant is quickly cleared from the mouth. In contrast, the smooth variant is able to invade oral epithelial cells in vitrobetter than the rough variant. It is hypothesized that the rough phenotype may initiate colonization and the smooth variant may enhance tissue damage through invasion of epithelial cells in the gingival crevice.
The aims of this project are to examine the differential expression of genes by the rough and smooth variants by microarrays and proteomics 1) to identify adhesins other than fimbriae involved in biofilm formation and 2) to identify global regulatory networks involved in biofilm formation.