Keywords: k. host/pathogen interactions; o. molecular interactions
Parasitic nematodes are an ongoing problem for human health and agriculture. Key to their success in
infection is the ability to evade or suppress host immunity. This immunomodulatory ability is likely due
to the release of hundreds of excretory/secretory proteins (ESPs) upon infection. While ESPs have been
shown to display immunosuppressive effects on a host, there are still gaps in understanding about the
molecular interactions between individual proteins released and host immunity. Our lab has recently
identified a secreted phospholipase A2 (sPLA2) released from the entomopathogenic nematode (EPN)
Steinernema carpocapsae, which has immunosuppressive and toxic capabilities in insects.
Immunosuppression by Sc-sPLA2 is characterized by its ability to suppress the toll pathway and
phagocytosis which lead to a decrease in survival against bacterial infections, and an increase in
pathogenic bacterial growth in an infection model. Toxicity by Sc-sPLA2 is characterized by increased
mortality, with the severity being both dose and time dependent. EPNs have homology to vertebrate-
parasitic nematodes, and thus can be used as model systems for understanding how nematode ESPs
alter host immunity. sPLA2 enzymes specifically, are known to be modulators of host immunity via lipid
signaling. Understanding how Sc-sPLA2 suppresses D. melanogaster host immunity will help elucidate
EPN immunomodulation at the molecular level and may increase our understanding of the role of lipid
signaling in insect immunity, which is an understudied aspect of the insect immune response.