Fig. 7.

Model for the role of H₂O₂ as a mediator of A. actinomycetemcomitans resistance to innate immunity. Enhanced levels of H₂O₂ produced by S. gordonii during plaque growth stimulate inflammation, leading to an influx of innate immune modulators, including complement and neutrophils. A. actinomycetemcomitans responds to rising H₂O₂ by induction of katA and apiA, which, in turn, enhance resistance to innate immune effectors. On recruitment to the site of inflammation, neutrophils increase the levels of H₂O₂ and further stimulate induction of katA and apiA.