Porphyromonas gingivalis galEIs Involved in Lipopolysaccharide O-Antigen Synthesis and Biofilm Formation

Abstract

Porphyromonas gingivalisis a crucial component of complex plaque biofilms that form in the oral cavity, resulting in the progression of periodontal disease. To elucidate the mechanism of periodontal biofilm formation, we analyzed the involvement of several genes related to the synthesis of polysaccharides inP. gingivalis. Gene knockoutP. gingivalismutants were constructed by insertion of anermF-ermAMcassette; among these mutants, thegalEmutant showed some characteristic phenotypes involved in the loss of GalE activity. As expected, thegalEmutant accumulated intracellular carbohydrates in the presence of 0.1% galactose and did not grow in the presence of galactose at a concentration greater than 1%, in contrast to the parental strain. Lipopolysaccharide (LPS) analysis indicated that the length of the O-antigen chain of thegalEmutant was shorter than that of the wild type. It was also demonstrated that biofilms generated by thegalEmutant had an intensity 4.5-fold greater than those of the wild type. Further, thegalEmutant was found to be significantly susceptible to some antibiotics in comparison with the wild type. In addition, complementation of thegalEmutation led to a partial recovery of the parental phenotypes. We concluded that thegalEgene plays a pivotal role in the modification of LPS O antigen and biofilm formation inP. gingivalisand considered that our findings of a relationship between the function of theP. gingivalis galEgene and virulence phenotypes such as biofilm formation may provide clues for understanding the mechanism of pathogenicity in periodontal disease.