239A Poster - 02. Immunity and the microbiome
Thursday April 07, 2:00 PM - 4:00 PM

Authors:
Andrea Darby ¹; Destiny Okoro ¹; Brian Lazzaro ^1,2

Affiliations:
1) Cornell University; 2) Cornell Institute of Host-Microbe Interactions and Disease

Keywords:
c. innate immunity; c. nutrition

An organism’s diet is a critical factor for its ability to survive an infection, and overnutrition of dietary sugar in particular has been demonstrated to increase susceptibility to infection across animal models and humans. Adult Drosophila melanogaster reared on high sugar diets experience higher bacterial burdens and higher mortality post infection, although the genetic and physiological mechanisms that lead to this outcome are not well understood. Prior studies that have investigated the impact of high dietary sugar on survival of infection have been performed using flies that that fed on high-sugar diets throughout their entire life, thus making it difficult to distinguish developmental consequences from acute metabolic effects on immunity. We hypothesized that even transient exposure to high-sugar diet might cause metabolic dysregulation with adverse consequence for immune function. To test this hypothesis, we reared D. melanogaster on a standard 4% (w/v) sucrose diet, then transferred them to one of six experimental diets varying from 0% - 24% sucrose upon eclosion. After 3-5 days of feeding, we assayed their infection survival over five days against systemic infection with two Gram-negative bacteria, Providencia rettgeri and Serratia marcescens, and one Gram-positive bacteria, Enterococcus faecalis. I found that even three days of exposure to elevated sugar in the diet was sufficient to significantly reduce the probability of surviving infection. However, this effect was specific to the Gram-negative bacteria assayed, suggesting that the immediate metabolic effects of high sugar may have disproportionate impact on the immune pathways that are required for combating Gram-negative infection. In ongoing work, we are testing infection survival in other Gram-positive bacteria, like Lactococcus lactis, to determine whether the sugar content affect is specific to Gram-negative bacteria. Additionally, we are testing whether elevated dietary sucrose specifically impairs IMD pathway signaling, and the extent to which different pathogens may themselves have different sensitivities to the excess sugar within their host. These results are foundational for further understanding of the genetic and physiological mechanisms by which high sugar impacts infection survival.