Abstract

As with other pathogens, a requirement for the in vivo growth of Porphyromonas gingivalis is that the organism must be capable of obtaining iron from the host. The ability to utilize hemin and hemin-containing compounds for nutritional iron has been documented for several pathogenic bacteria, including P. gingivalis; however, the mechanisms involved in hemin uptake are poorly defined. I have determined that P. gingivalis transports the entire hemin moiety into the cell by an energy-dependent mechanism and that the binding and accumulation of hemin are induced by growth of cultures in the presence of hemin. A model of hemin transport in P. gingivalis consistent with these results is presented. I have also found that, in P. gingivalis, hemin regulates the expression of several putative virulence factors; this in turn results in the increased virulence potential of P. gingivalis as assessed in an animal model. Regulation of hemin-responsive genes in P. gingivalis may occur by a negative regulator, as has been described in other pathogenic organisms.

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