Fig. 4.

The A. actinomycetemcomitans oxyR⁻ mutant is hypersusceptible to killing by H₂O₂ and human serum. (A) The H₂O₂ minimum inhibitory concentration (lowest concentration necessary to inhibit visible growth of an organism) of WT A. actinomycetemcomitans (wt), the A. actinomycetemcomitans oxyR⁻ mutant (oxyR⁻), and the genetically complemented A. actinomycetemcomitans oxyR⁻ mutant (oxyR⁻ + oxyR). (Inset) RT-PCR analysis of mRNA levels of katA and the clpX constitutively expressed control in the wt oxyR⁻, and oxyR⁻ + oxyR after H₂O₂ exposure. (B) Survival of wt, oxyR⁻, oxyR⁻ + oxyR, and oxyR⁻ constitutively expressing apiA (oxyR⁻ + apiA) in the presence of 50% (vol/vol) normal human serum. Percent survival was calculated as follows: number of cells recovered from normal human serum treatment/number of cells recovered from heat-inactivated serum treatment. (Inset) RT-PCR analysis of mRNA levels of apiA and the clpX constitutively expressed control in the wt, oxyR⁻, and oxyR⁻ + oxyR after H₂O₂ exposure. As a control, exogenous catalase was added to serum to ensure that any phenotype observed was not attributable to endogenous H₂O₂ within serum. Error bars represent SEM. *P < 0.004 via Student's t test, n = 3.