Bacterial metabolism during infection is related to bacterial persistence and virulence factors. Porphyromonas gingivalis is a key pathogen that contributes to chronic periodontitis. Our previous study showed that pckA, the gene encoding phosphoenolpyruvate carboxykinase, is a putative-specific pathogenic gene of virulent strains of P. gingivalis. Here, a pckA-deficient strain (ΔPG1676) was constructed in P. gingivalis W83. Virulence properties were compared between the mutant and wild-type strains. Specifically, hemagglutination activity was determined by the ability to agglutinate sheep erythrocytes. Gingipain activity was detected using synthetic-specific substrates. Gene expression levels were analyzed using RT-qPCR, and cell surface-associated polysaccharides were examined by silver staining and electron microscopy. Inactivation of the pckA gene did not affect bacterial growth and lipopolysaccharide formation but led to a reduction in hemagglutination activity and downregulation in expression of the hemagglutination-associated gene, rfa, when compared with the wild-type strain. Additionally, the ΔPG1676 mutant exhibited an alteration in the distribution of gingipain activity. Increased gingipain activity was detected on the cell surface, but a decrease in its activity in the culture supernatant was shown. Taken together, our results suggest that the pckA gene plays a role in modulating the virulence of P. gingivalis W83.
Keywords: chronic periodontitis; pathogen; phosphoenolpyruvate carboxykinase; virulence factors.
© 2018 Eur J Oral Sci.