![]() reported that, among different highly transformable S. pneumoniae to repair the oxidative DNA damages in its genome, caused by this host defense, likely contributes to this pathogen’s virulence. pneumoniae infection stimulates polymorphonuclear leukocytes (granulocytes) to produce an oxidative burst that is potentially lethal to the bacteria. On the basis of these findings, they suggested that transformation is an adaptation for repairing oxidative DNA damages. ![]() pneumoniae is associated with increased resistance to oxidative stress and increased expression of the RecA protein, a key component of the recombinational repair machinery for removing DNA damages. summarized evidence that induction of competence in S. pneumoniae against the bactericidal effect of mitomycin C. pneumoniae is induced by DNA-damaging agents such as mitomycin C, fluoroquinoloneantibiotics (norfloxacin, levofloxacin and moxifloxacin), and topoisomerase inhibitors.
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