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ARS Home » Midwest Area » Columbia, Missouri » Biological Control of Insects Research » Research » Publications at this Location » Publication #194470


item Stanley, David

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 4/21/2006
Publication Date: 5/24/2006
Citation: Stanley, D.W. 2006. Eicosanoids mediate insect cellular immunity [abstract]. 2nd International Conference on Non-Mammalian Eicosanoids, Bioactive Lipids and Plant Oxylipins. p. 32.

Interpretive Summary:

Technical Abstract: Insects express innate, but not adaptive, immune reactions to infection and invasion. These innate responses are for convenience seen as humoral or cellular reactions. Humoral reactions involve regulated expression of genes encoding a wide range of anti-bacterial and anti-fungal proteins which appear in hemolymph 6 to 12 h post-infection (PI). Cellular immunity entails direct interactions between circulating hemocytes and invaders. These interactions, launched immediately when an infection is detected, include phagocytosis, nodulation, and for organisms too large to be internalized, encapsulation. Nodulation is a multi-step process of attaching invading cells or spores to hemocytes. The hemocytes attach to one another, forming microaggregates, which grow into nodules. The nodules are finally melanized and attached to internal surfaces, where the invaders are secondarily killed by oxygen-dependent mechanisms. Nodulation is responsible for clearing from circulation nearly all invading cells within 2 h PI. Using selective inhibitors of PLA2, COX and LOX, we demonstrated that eicosanoids are crucial mediators of cellular immune reactions to invasions by bacteria, fungi and parasitoids. We also reported that bacterial challenge led to increased hemocytic PLA2 activity and increased hemolymph PG titres in experimental insects. Some microbial pathogens have usurped eicosanoid-mediate immune reactions. The bacterium, Xenorhabdus nematophila, is an extraordinarily potent insect pathogen. We learned that part of the pathogenicity is due to secretion of bacterial factors that inhibit eicosanoid biosynthesis. The factors specifically target sPLA2s responsible for releasing eicosanoid-precursor fatty acids from PLs. This mechanism may operate in many pathogens, as the protozoan parasite, Trypanosoma rangeli, seems to inhibit eicosanoid-mediated immunity in the blood-sucking bug, Rhodnius prolixus, a major disease vector in South America. These observations indicate that eicosanoids play an important role in insect immunity to pathogens.