Poster Title (Current Submission)

Development of A Pulmonary Bacterial Model for Testing the Immune Factors Contributing to the Increased Pulmonary Disease Observed in Alcoholics

Major(s)

Microbiology, Biochemistry

Mentor Name

Kevin Legge

Mentor Department

Pathology, Microbiology

Abstract

Epidemiology studies have shown a clear correlation between chronic consumption of alcohol and increases the incidence and severity of pulmonary infections. Consistent with these findings, our own recent studies using an animal model have demonstrated that chronic alcohol consumption leads to increased mortality, viral titers, pulmonary edema, and neutrophilia as well as significantly reduced virus specific CD8 T cell response during influenza virus infections. Together our results suggested that chronic alcohol alters both the innate and adaptive arms of the immune response therein contributing to the increased disease severity. In order to determine if these findings were unique to influenza virus infections or are more universal we are developing a pulmonary bacteria infection model. To this end chronic ethanol consuming or water control mice will infected with Streptococcus, the most common bacteria associated with pneumonias in alcoholics, and the immune response, pulmonary inflammation, and disease severity monitored. Completion of this study should allow us to define common pathways that enhance pulmonary disease severity in alcoholics and therein offer potential targets for drug interventions.

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Development of A Pulmonary Bacterial Model for Testing the Immune Factors Contributing to the Increased Pulmonary Disease Observed in Alcoholics

Epidemiology studies have shown a clear correlation between chronic consumption of alcohol and increases the incidence and severity of pulmonary infections. Consistent with these findings, our own recent studies using an animal model have demonstrated that chronic alcohol consumption leads to increased mortality, viral titers, pulmonary edema, and neutrophilia as well as significantly reduced virus specific CD8 T cell response during influenza virus infections. Together our results suggested that chronic alcohol alters both the innate and adaptive arms of the immune response therein contributing to the increased disease severity. In order to determine if these findings were unique to influenza virus infections or are more universal we are developing a pulmonary bacteria infection model. To this end chronic ethanol consuming or water control mice will infected with Streptococcus, the most common bacteria associated with pneumonias in alcoholics, and the immune response, pulmonary inflammation, and disease severity monitored. Completion of this study should allow us to define common pathways that enhance pulmonary disease severity in alcoholics and therein offer potential targets for drug interventions.