UC Irvine

Insects, like any other organisms, are in constant contact with pathogenic biotic elements in their environment. Though they only possess an innate immune response (which is typically considered a non-specific and short-lived response to infection), immune memory from previous infections has been observed in insects. Innate immune priming increases an organism’s survival of a second infection after an initial, non-lethal infection. We used Drosophila melanogaster and an insect-derived strain of Enterococcus faecalis to study transcriptional, physiological, and temporal control of priming. In contrast to work with other pathogens, the enhanced survival in primed animals does not correlate with decreased bacterial load, and further analysis shows that primed organisms tolerate, rather than resist infection. Using RNA-seq of immune tissues, we found many genes were up-regulated in only primed flies. In contrast, few genes continuously express throughout the experiment or more efficiently re-activate upon reinfection. Priming experiments in immune deficient mutants revealed Imd signaling is largely dispensable for responding to a single infection but needed to fully prime. The fly’s innate immune response is plastic — differing in immune strategy, transcriptional program, and pathway use depending on infection history. We explore this plasticity by varying infecting pathogens, re-infection times, and host genotype. Ability to prime against Enterococcus faecalis re-infection was dependent on host genotype and the rest time between exposures. Although there was no homologous priming with Serratia marcescens, heterologous priming between E. faecalis and S. marcescens was observed. Immune priming is not a static phenotype – it is highly dependent on assay and environmental conditions.