Understanding the insect immune responses to Yersinia pestis using Drosophila melanogaster

Abstract

Yersinia pestis, the causative agent of plague, continues to be transmitted in many different continents, most often by fleas. Despite knowing for a century that Y. pestis can form a biofilm on the flea's proventriculus while its closest relatives do not, it is still poorly understood what transmission factors permit this colonization. A growing collection of work is beginning to identify components of the flea's immune response to Y. pestis infection and the ways in which Y. pestis evades this response. It has also previously been established that lipooligosaccharide (LOS) mutants are unable to form a blockage in the flea midgut. The LOS mutants colonize the flea, but not at the proventriculus where wild-type Y. pestis grows, perhaps due to a heightened sensitivity to the flea immune response. Here it is shown that LOS is required for early survival in the flea. New models are described using Drosophila melanogaster to get a more precise look at the interaction between Y. pestis and insect immune cells. A novel cytotoxic effect of Y. pestis on insect immune cells is highlighted. Finally, autophagy is shown to be an important aspect of the insect immune response to Y. pestis infection.