Effects of Chronic Alcohol and Glucose Exposure on Viability of Alveolar Macrophages

Abstract

The general population widely acknowledges the potential adverse health risks associated with the lifestyle factors of chronic alcohol abuse and obesity. These factors are manifested in the form of routine elevated blood ethanol and glucose levels, respectively. There is evidence which shows that the lungs are secondary organs affected by such physiological conditions. Healthy lungs are protected against infection and harmful airborne particles by macrophages— one of the working entities of the immune system. However, when these immune-responsive cells are compromised and unable to adequately perform normal functions, lung health may deteriorate. Therefore, a healthy pulmonary alveolar macrophage population is vital for the preservation of adequate lung function and for the prevention of respiratory infections and related complications. Chronic alcohol exposure and elevated glucose concentrations have been shown to suppress alveolar macrophage function, in turn possibly lowering the lungs’ first line of defense against foreign particles and infection. The objective of this study is to determine the effects of exogenous ethanol and increased glucose concentration on macrophage size and viability in relation to their compromised functionality within the human system through an in vitro study. This study tested alveolar macrophage response to conditions of elevated glucose levels, exogenous ethanol, and a joint treatment in a laboratory setting. Elevated glucose levels were representative of hyperglycemic conditions which often occur in states of obesity, while ethanol treatment simulated chronic alcohol exposure. NR8383 rat alveolar macrophages were grown in vitro in 25 cm3 flasks with each treatment. In addition to treatments, a control was maintained to ensure integrity of the experiment. Each conditional treatment was subjected to weekly viability testing and imaging for size analysis. The data was compared among the different treatment groups to gain a better understanding of how alveolar macrophages were affected by the specified conditions. The hypothesized theory anticipates an increased cell count in the glucose treated cells, but a decreased cell count in the ethanol and combination treatments. All three treatments were expected to yield smaller cell size, thus impairing macrophage function. Future studies plan to expose each treatment group to the bacterial agent lipopolysaccharide, or LPS, to test the initiated response of the macrophages and determine levels of functionality. LPS is commonly found on the outer membrane of gram-negative bacteria and is a reliable stimulant of the mammalian immune system. Differential responses of the treatment groups to LPS will indicate the overall health and functionality of the macrophages, helping to determine the effects that chronic alcohol and glucose exposure manifest on alveolar macrophages. Results from the current experiment will be analyzed to hypothesize clinically relevant responses.