Host Immune Priming and Entomopathogenic Nematode Infectivity
CHRISTOPHER JACOBS1 and CHRISTOPHER HARVEY2
1,2Canterbury Christchurch University North Homes Road, Canterbury, Kent CT1 1QU, United Kingdom
ABSTRACT
  Entomopathogenic nematodes (EPNs) have a wide host range in the laboratory and the potential to be an effective biological control agent for insect pests. Field applications of nematodes have been met with mixed success, however. For EPNs to become more practically viable we need to understand the interactions between the nematodes, their hosts and the environment. A wide range of stress factors have been shown to cause an immune priming effect in insects which may affect EPN infectivity.
  Physical stress, temperature, desiccation and nutrient levels have been shown to elicit stress responses in insects that can affect  immune response to pathogen infection. Measuring the bioluminescence of host insects infected by Heterorhabditis species will allow a quantitative measure of infection rates in hosts under different stress conditions. Using western blotting of stress-related proteins (e.g. heat-shock proteins), we will  identify whether  upregulation of stress proteins (as an indicator of stress response) is associated with immune priming. Looking at  physiological changes, such as  levels will allow us to investigate the effects of stress on immune cell levels in insects and immune priming and how this affects susceptibility to nematode  infection.
  To date most of the research into immune priming has been focused on the use of bacteria (Bacillus thuringiensis) and entomopathogenic fungi but its effects on EPN infectivity are relatively unexplored. Understanding the conditions that cause immune priming in insects and the effect it has on EPN infectivity will allow us to predict  optimal timing of nematode application for biological control  based on insect stress levels and will allow us to better evaluate the results of laboratory-based studies and to what extent they benefit the situation in the field.