EICOSANOID-MEDIATED AND MOLECULAR IMMUNE SIGNALING INHIBITORS IN PIERCING/SUCKING INSECT PESTS OF SMALL AND URBAN VEGETABLE FARMS
Location: Biological Control of Insects Research
Title: Plasmatocyte spreading peptide influences hemocyte behavior via eicosanoids
Submitted to: Archives of Insect Biochemistry and Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 30, 2011
Publication Date: November 1, 2011
Citation: Srikanth, K., Park, J., Stanley, D.W., Kim, Y. 2011. Plasmatocyte spreading peptide influences hemocyte behavior via eicosanoids. Archives of Insect Biochemistry and Physiology. 78:145-160.
Interpretive Summary: Application of classical insecticides has introduced severe problems in agricultural sustainability. The concept of biological control of insects is a potentially powerful alternative to classical insecticides. Biological control is based on the idea that direct application of insect-specific pathogens and parasites can reduce pest insect populations and the economic damage due to pest insects. The problem, however, is the efficiency of these organisms in biological control programs is limited by insect immune defense reactions to challenge. One approach to improving the efficiency of biocontrol agents would be to somehow disable insect immune reactions to viral, bacterial, fungal and parasitic infections. With this goal, we are investigating how insect immune reactions to infection are signaled. In this paper we report on identification of crosstalk between two entirely different biochemical signals responsible for stimulating insect defenses to infection. This new research will be directly useful to scientists who are working to improve the efficacy of biological control methods. The ensuing improved biological control methods will benefit a wide range of agricultural producers by supporting the long-term sustainability of agriculture.
Insect innate immunity is composed of humoral and hemocytic (or cellular) responses. Humoral responses involve induced biosynthesis of anti-microbial proteins and cellular responses are characterized by direct interactions between hemocytes (mainly granulocytes and plasmatocytes) and invading microbes. Nodulation is the quantitative predominant defense action, which clears the vast majority of invading microbes from circulation. The nodulation response is completed by a layer of plasmatocytes which spread over the nodule and initiate a malanization process leading to darkened nodules. Plasmatocyte spreading peptide (PSP), the first reported insect cytokine, is responsible for mediating the spreading and attachment of some sub-classes of plasmatocytes to nodules. Prostaglandins (PGs), one group of eicosanoids formed from arachidonic acid (AA), also mediate plasmatocyte spreading (PS), although the potential interactions between the PSP and PG signal transduction pathways have not been investigated. We tested our hypothesis that PSP acts via biosynthesis of eicosanoids, specifically PGs, in the beet armyworm, Spodoptera exigua. Here we report that 1/ PSP and PGE2 independently stimulated Ca++-dependent PS, 2/ that inhibitors of PG biosynthesis reversibly blocked PS, 3/ that dsRNA silencing the gene encoding proPSP blocked PS, which was rescued by PSP and by AA, 4/ that PSP-stimulated PS was reversibly impaired by inhibitors of PG biosynthesis, and 5/ the inhibitor-impaired spreading was rescued by AA. Taken together, these points strongly support our model showing that PSP acts via a plasmatocyte-surface receptor, which stimulates biosynthesis of the PGs responsible for mediating plasmatocytes spreading.