Hemagglutinin B Is Involved in the Adherence of Porphyromonas gingivalis to Human Coronary Artery Endothelial Cells

Abstract

Porphyromonas gingivalis is a periodontopathogen that may play a role in cardiovascular diseases. Hemagglutinins may function as adhesins and are required for virulence of several bacterial pathogens. The aim of this study was to determine the role of hemagglutinin B (HagB) in adherence of P. gingivalis to human coronary artery endothelial (HCAE) cells. P. gingivalis strain 381, a P. gingivalis 381 HagB mutant, Escherichia coli JM109 expressing HagB (E. coli-HagB), and E. coli JM109 containing pUC9 (E. coli-pUC9) were tested for their ability to attach to HCAE cells. Inhibition assays were performed to determine the ability of purified recombinant HagB (rHagB) as well as antibodies to HagB, including the polyclonal antibody (PAb) A7985 and the monoclonal antibody (MAb) HL1858, to inhibit the attachment of P. gingivalis to HCAE cells. As expected, when the attachment of P. gingivalis and the HagB mutant were compared, no statistical significance was observed between the two groups (P ‫؍‬ 0.331), likely due to the expression of the hagB homolog hagC. However, E. coli-HagB adhered significantly better to HCAE cells than did E. coli-pUC9, the control strain. In a competition assay, the presence of purified rHagB decreased bacterial adhesion of P. gingivalis or E. coli-HagB to HCAE cells. The presence of PAb A7985 or MAb HL1858 also significantly decreased attachment of P. gingivalis and E. coli-HagB to host cells. These results indicate that HagB is involved in the adherence of P. gingivalis to human primary endothelial cells.

E-Selectin Mediates Porphyromonas gingivalis Adherence to Human Endothelial Cells

“…gingivalis interacts with TNF-␣-stimulated endothelial cells via Pgm6/7. The initial adherence of P. gingivalis to host cells is mediated by multiple adhesins, including FimA and HagB (44,45). To determine whether an interaction occurs between the major fimbriae and E-selectin, we examined adherence to endothelial cells of P. gingivalis defective in FimA alone (⌬FimA).…”

The Role of Oral Pathobionts in Dysbiosis during Periodontitis Development

“…Similarly, structural analysis of biofilms in vivo and co-aggregation analysis in vitro with periodontitis-associated bacteria provided evidence that physiological interactions of red complex bacteria with non-red complex bacteria facilitate their colonization (Jenkinson and Lamont, 2005). Periodontitis-associated bacteria express several putative adhesins, and Pg produces hemagglutinins that are important for the interaction of bacteria with host cells or bacterial invasion into host cells (Song et al, 2005). Similarly, Flp fimbriae, YadA-containing ApiA/Omp100, and two non-fimbriae autotransporter proteins, EmaA and Aae, are important for the interaction of Aa with host factors and/or host cells (Henderson et al, 2010).…”

Autophagy: A Highway for Porphyromonas gingivalis in Endothelial Cells

“…17 The initial adherence of P. gingivalis to host cells is mediated by multiple adhesins including FimA and HagB. [18][19][20][21][22] However, our knowledge of the initial events of P. gingivalis internalization is limited, especially with regard to internalization into HCAEC. There is some evidence that interaction with lipid rafts may serve as a portal of entry for P. gingivalis into host eukaryotic cells.…”