White-Nose Syndrome Disrupts the Splenic Lipidome of Little Brown Bats (Myotis lucifugus) at Early Disease Stages

White-nose syndrome (WNS)-positive
little brown bats (Myotis lucifugus) may exhibit immune responses including
increased cytokine and pro-inflammatory mediator gene levels. Bioactive
lipid mediators (oxylipins) formed by enzymatic oxidation of polyunsaturated
fatty acids can contribute to these immune responses, but have not
been investigated in WNS pathophysiology. Nonenzymatic conversion
of polyunsaturated fatty acids can also occur due to reactive oxygen
species, however, these enantiomeric isomers will lack the same signaling
properties. In this study, we performed a series of targeted lipidomic
approaches on laboratory Pseudogymnoascus destructans-inoculated bats to assess changes in their splenic lipidome, including
the formation of lipid mediators at early stages of WNS. Hepatic lipids
previously identified were also resolved to a higher structural detail.
We compared WNS-susceptible M. lucifugus to a WNS-resistant species, the big brown bat (Eptesicus
fuscus). Altered splenic lipid levels were only observed
in M. lucifugus. Differences in splenic
free fatty acids included both omega-3 and omega-6 compounds. Increased
levels of an enantiomeric monohydroxy DHA mixture were found, suggesting
nonenzymatic formation. Changes in previously identified hepatic lipids
were confined to omega-3 constituents. Together, these results suggest
that increased oxidative stress, but not an inflammatory response,
is occurring in bats at early stages of WNS that precedes fat depletion.
These data have been submitted to metabolomics workbench and assigned
a study number ST002304.