New insights into active oxygen metabolism during bacterial pathogenesis

The hypersensitive response (HR) is considered to be a defense response involving rapid plant cell death which localizes pathogenic microbes and prevents their spread throughout the plant. Hypersensitive cell death in either intact leaves or cell suspensions occurs at 10 to 15 h after treatment with incompatible (HR-causing) bacteria. Within the first few hours, a two-phased production of Active oxygen (AO) unique to incompatible responses is detectable. Although reports have suggested that this AO burst itself may be responsible for the necrosis associated with HR, we have found bacterial mutants that are able to cause the AO burst but not the HR. Other reports have suggested that the H2O2 produced during pathogenesis may be inhibitory to bacterial pathogens and that stationary phase bacteria cells are more tolerant of H2O2 due to their increased levels of catalase. However, we have recently demonstrated that due to the high permeability of H2O2 through the bacterial membrane, it is the bacterial cell concentration rather than catalase level that is critical to pathogen survival. In addition, in interactions between bacteria and cell suspensions, catalase is only minimally advantageous in regard to scavenging H2O2 due to the high Km of catalase (>100 mM) and the low levels of H2O2 encountered in cell suspension systems (<100 mu M).