Abstract
Aggregatibacter actinomycetemcomitans a causative agent of periodontal disease in humans, forms biofilm on biotic and abiotic surfaces. A. actinomycetemcomitans biofilm is heterogeneous in nature and is composed of proteins, extracellular DNA and exopolysaccharide. To explore the role played by the exopolysaccharide in the colonization and disease progression, we employed genetic reduction approach using our rat model of A. actinomycetemcomitans-induced periodontitis. To this end, a genetically modified strain of A. actinomycetemcomitans lacking the pga operon was compared with the wild-type strain in the rat infection model. The parent and mutant strains were primarily evaluated for bone resorption and disease. Our study showed that colonization, bone resorption/disease and antibody response were all elevated in the wild-type fed rats. The bone resorption/disease caused by the pga mutant strain, lacking the exopolysaccharide, was significantly less (P < 0.05) than the bone resorption/disease caused by the wild-type strain. Further analysis of the expression levels of selected virulence genes through RT-PCR showed that the decrease in colonization, bone resorption and antibody titer in the absence of the exopolysaccharide might be due to attenuated levels of colonization genes, flp-1, apiA and aae in the mutant strain. This study demonstrates that the effect exerted by the exopolysaccharide in A. actinomycetemcomitans-induced bone resorption has hitherto not been recognized and underscores the role played by the exopolysaccharide in A. actinomycetemcomitans-induced disease.
Highlights
It has been well documented that biofilm bacteria predominate, numerically and metabolically, in virtually all nutrient-sufficient ecosystems, including the oral cavity [1,2]
The exopolysaccharide of Aggregatibacter actinomycetemcomitans (PGA) is a homopolymer of N-acetyl-D-glucosamine residues in β(1,6) linkage and has been well characterized in several bacteria including Staphylococcus aureus, S. epidermidis and E. coli. This exopolysaccharide has been named differently in various bacteria but its synthesis is encoded by a set of four genes, icaADBC in Staphylococcal species and pgaABCD in E. coli and A. actinomycetemcomitans
We have focused our attention on the oral bacterium A. actinomycetemcomitans that is a causative agent of localized aggressive periodontitis (LAP)
Summary
It has been well documented that biofilm bacteria predominate, numerically and metabolically, in virtually all nutrient-sufficient ecosystems, including the oral cavity [1,2]. Role of Exopolysaccharide in Bone Resorption polymeric substance), which holds the cells together and firmly attaches the bacterial cells to the underlying surface [3]. The extracellular polymeric substance has been attributed to a protective role as well as it is a source of dissolved nutrients, secreted enzymes, extracellular DNA and exopolysaccharide. The exopolysaccharide of Aggregatibacter actinomycetemcomitans (PGA) is a homopolymer of N-acetyl-D-glucosamine residues in β(1,6) linkage and has been well characterized in several bacteria including Staphylococcus aureus, S. epidermidis and E. coli. This exopolysaccharide has been named differently in various bacteria but its synthesis is encoded by a set of four genes, icaADBC in Staphylococcal species and pgaABCD in E. coli and A. actinomycetemcomitans. PGA may act through a general mechanism wherein it binds to or electrostatically repulses immune modulators and antimicrobial agents, thereby preventing their access to the bacterial cell [5]
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