| Summary: | The disease periodontitis is an inflammatory response to the oral bacterial microflora. The Gram-negative bacterium Aggregatibacter actinomycetemcomitans has been specifically associated with the aggressive type of periodontitis. This species has a number of virulence factors that can contribute to host cell death, tissue inflammation, bone resorption, and colonization advantage relative to other microbes. A. actinomycetemcomitans has defense mechanisms against killing by the complement system (a part of our immune system). In the alternative pathway of complement activation, a protein called Factor H is the main regulator by having the ability to inhibit the complement reactions in three separate ways. Binding of Factor H to the bacterial surface was earlier shown to promote survival in human serum of an A. actinomycetemcomitans serotype d strain. This binding was caused by the outer membrane protein Omp100. The aim of this study was to establish whether Omp100 has a similar role in other serotypes of A. actinomycetemcomitans. For this we examined the serotype a strains D7S and D7SS, and their omp100 knockout mutants, which were generated in this laboratory. Western immunoblotting was used to compare a possible amount difference of the protein in each serotype. By incubating the bacterial strains in human serum, our results showed that lack of Omp100 did not have an obvious negative effect on the serum survival rate in strain D7S nor D7SS. We therefore concluded that omp100 was not required for serum resistance in these serotype a strains, and suggest that there might be another protein or factor in this serotype that is more important for serum resistance.
|
|---|
