It was recently shown that, as in yeast, alcohols selectively increase the hemolytic properties of certain staphylococci strains. This phenomenon has been called 'microbial alcohol-conferred hemolysis'(MACH). Here we present the changes in gene expression by Staphylococcus aureus 8325-4, in response to ethanol. Ethanol upregulated the expression of multiple toxins and increase the pathogen potential of S. aureus strain 8325-4. Ethanol also increased the level of genes considered necessary for production and viability of biofilm, such as: icaAD, sdrDE, pyr, and ure. Increased urease activity appeared to be an important factor in the ethanol response along with macromolecule repair mechanisms. Oxidative-stress responses, such as increased expression of sodA1, sodA2 and upregulation of zinc-containing alcohol dehydrogenase, alcohol-acetaldehyde dehydrogenase (adhE) and two aldehyde dehydrogenases (aldA1, aldA2), which can generate more reducing power, were also induced. Upregulation of fatty acid metabolism appears to be important in enabling the bacteria to handle excess amounts of ethanol which ultimately may lead to synthesis of lytic lypids. The patterns of regulation were confirmed by quantitive reverse transcriptase PCR (QRT-PCR). These results, taken together, suggest that exposure to ethanol increases pathogenic traits and induce oxidative-stress responses.
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