Submitted to: Southeast Regional Society of Toxicology
Publication Type: Abstract only
Publication Acceptance Date: 10/5/2005
Publication Date: 10/19/2005
Citation: Stanley, D.W. 2005. A novel pathogenic mechanism in an insect bacterium: secretion of phospholipase A2 inhibitors [abstract]. Southeast Regional Society of Toxicology. p. 16. Interpretive Summary:
Technical Abstract: The bacterium Xenorhabdus nematophila is a mutualistic partner of the entomopathogenic nematode Steinernema carpocapsae. Juvenile forms of the nematode enter a host insect and release its bacterial partner into the hemocoel, where the bacteria multiply and kill the host. The freshly-killed insect is an ideal micro-environment for nematode development and reproduction. Insects express robust innate immune reactions to bacterial infection, including hemocytic (immediate) and humoral (6 to 12 hr post-infection) reactions. Hemocytic reactions include phagocytosis and nodulation (melanized aggregates of hemocytes and bacterial cells) and humoral reactions involve induced biosynthesis of anti-bacterial proteins. Innate insect immune functions are efficacious and could disrupt the bacterium-nematode relationship. To the contrary, X. nematophila directs several mechanisms toward impairing insect immunity. These include killing of hemocytes, inhibition of anti-bacterial protein expression and disabling hemocytic immune functions. Insect cellular immune reactions are mediated by various eicosanoids and X. nematophila impairs insect cellular immunity by inhibiting eicosanoid biosynthesis. Insect hemocytes express cellular and secretory forms of PLA2. The bacterium inhibits insect cellular immunity by inhibiting hemocytic secretory PLA2 (sPLA2). Heat-labile factors partially purified from organic extracts of X. nematophia culture medium are responsible for inhibiting sPLA2s. These factors similarly inhibit several sPLA2s, including insect and reptile venom PLA2s and pancreatic PLA2. Inhibition of sPLA2 activity disables cellular immune reactions and thereby protects both the infecting bacteria and its symbiotic nematode from insect defenses during the time between nematode infection and death of the host insect.