The Effect of Acetate on Listeria monocytogenes Pathogenesis

Affecting 1 in 6 Americans annually, foodborne illnesses range from mild gastroenteritis, to life- threatening conditions in high risk individuals with weakened immune systems. Those with chronic alcohol dependency fall in to the last category. Research on elucidating the mechanism of alcohol toxicity has focused on the intermediate of alcohol metabolism: acetaldehyde. However, it is not clear if acetate, the final product of alcohol metabolism, plays any role in individual susceptibility to foodborne infections. Therefore, my research project aims to determine the role of acetate in foodborne infections by using the Gram-positive bacterium Listeria monocytogenes as the model foodborne pathogen and establishing the effects of acetate on Listeria pathogenesis. Listeria pathogenesis was assayed by two different methods. First, the production of the toxin listeriolysin O (LLO) was determined in Listeria culture supernatant by hemolytic assays. Second, the ability of Listeria to cause infections was determined using a cell culture-based infection model. My results showed that the presence of acetate (50mM) significantly increased the anaerobic LLO production but not aerobic LLO production, suggesting that oxygen is critical in modulating the effect of acetate on Listeria. My preliminary results on cell culture infections showed that Listeria grown with acetate had an equal or slightly less infection rate in macrophages. I plan to expand the cell culture infection work in the following year to address the effect of acetate on cell susceptibility to Listeria infections using a human colonic epithelial cell line as another relevant cell types. Together, we will obtain a more comprehensive understanding on how acetate influence Listeria-host interactions. In the long run, we hope to contribute to the development of treatments for chronic alcohol dependency to lessen the financial and medical burden of alcoholism on individuals and on the society