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The efficient clearance of microbes by neutrophils requires the concerted action of reactive oxygen species and microbicidal components within leukocyte secretory granules. Rubrerythrin (Rbr) is a nonheme iron protein that protects many air-sensitive bacteria against oxidative stress. Using oxidative burst-knockout (NADPH oxidase–null) mice and an  rbr  gene knockout bacterial strain, we investigated the interplay between the phagocytic oxidative burst of the host and the oxidative stress response of the anaerobic periodontal pathogen  Porphyromonas gingivalis.  Rbr ensured the proliferation of  P. gingivalis  in mice that possessed a fully functional oxidative burst response, but not in NADPH oxidase–null mice. Furthermore, the in vivo protection afforded by Rbr was not associated with the oxidative burst responses of isolated neutrophils in vitro. Although the phagocyte-derived oxidative burst response was largely ineffective against  P. gingivalis  infection, the corresponding oxidative response to the Rbr-positive microbe contributed to host-induced pathology via potent mobilization and systemic activation of neutrophils. It appeared that Rbr also provided protection against reactive nitrogen species, thereby ensuring the survival of  P. gingivalis  in the infected host. The presence of the  rbr  gene in  P. gingivalis  also led to greater oral bone loss upon infection. Collectively, these results indicate that the host oxidative burst paradoxically enhances the survival of  P. gingivalis  by exacerbating local and systemic inflammation, thereby contributing to the morbidity and mortality associated with infection.

Roles of the Host Oxidative Immune Response and Bacterial Antioxidant Rubrerythrin during Porphyromonas gingivalis Infection