Insects express 3 lines of protection from infections and invasions. Their cuticles and peritrophic membranes are physical barriers. Infections and invasions are quickly recognized within insect bodies, and recognition launches 2 lines of innate immune reactions. Humoral reactions involve induced synthesis of antimicrobial peptides, the bacteriolytic enzyme lysozyme and activation of the prophenoloxidase system. Cellular immune reactions include phagocytosis, nodulation and encapsulation. These reactions entail direct interactions between circulating hemocytes and the invaders. Cellular immune reactions begin immediately after an invasion is detected while antimicrobial peptides typically appear in the hemolymph some hours after infection. Microaggregation is a step in the nodulation process, which is responsible for clearing the bulk of bacterial infections from circulation. Coordinated cellular actions lead to encapsulation of invaders, such as parasitoid eggs, that are very much larger than individual hemocytes. In this paper, we review the roles of eicosanoids as central mediators of insect immune reactions, particularly cellular reactions. We briefly describe insect immune functions, outline eicosanoid biosynthesis and treat eicosanoid actions in cellular immunity of insects. Eicosanoids act in several cellular defense functions, including phagocytosis, microaggregation, nodulation, encapsulation, cell spreading and hemocyte migration toward a source of a bacterial peptide. We also describe our most recent work on the influence of one group of eicosanoids, prostaglandins, on gene expression in an established insect cell line.

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Nodulation is the first, and qualitatively predominant, cellular defense reaction to bacterial infections in insects. We tested the hypothesis that eicosanoids also mediate nodulation reactions to bacterial challenge in adults of a social insect, the honey bee, Apis mellifera. Treating newly-emerged experimental bees with the eicosanoid biosynthesis inhibitor, dexamethasone, impaired nodulation reactions to bacterial infections, and the influence of dexamethasone was reversed by treating infected insects with arachidonic acid, an eicosanoid precursor. Several other eicosanoid biosynthesis inhibitors, including the cyclooxygenase inhibitor, indomethacin, and the dual cyclooxygenase/lipoxygenase inhibitor, phenidone, also impaired the ability of experimental honeybees to form nodules in reaction to bacterial challenge. The influence of phenidone on nodulation was expressed in a dose-dependent manner. However, in experiments with older honey bees foragers, similar bacterial challenge did not evoke nodulation reactions. We infer from our results that while eicosanoids mediate cellular immune responses to bacterial infections in newly emerged honey bees, and more broadly, in most insect species, nodulation reactions to bacterial challenge probably do not occur in all phases of insect life cycles.

Intracellular phospholipase A(2) (PLA(2)) is responsible for releasing arachidonic acid from cellular phospholipids, and is thought to be the first step in eicosanoid biosynthesis. Intracellular PLA(2)s have been characterized in fat body and hemocytes from tobacco hornworms, Manduca sexta. Here we show that bacterial challenge stimulated increased PLA(2) activity in isolated hemocyte preparations, relative to control hemocyte preparations that were challenged with water. The increased activity was detected as early as 15 s post-challenge and lasted for at least 1 h. The increased activity depended on a minimum bacterial challenge dose, and was inhibited in reactions conducted in the presence of oleyoxyethylphosphorylcholine, a site-specific PLA(2) inhibitor. In independent experiments with serum prepared from whole hemolymph, we found no PLA(2) activity was secreted into serum during the first 24 h following bacterial infection. We infer that a hemocytic intracellular PLA(2) activity is increased immediately an infection is detected. The significance of this enzyme lies in its role in launching the biosynthesis of eicosanoids, which mediate cellular immune reactions to bacterial infection.

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Insect immunology is an active research arena, however, the vast majority of research in the area is conducted on model species taken from laboratory cultures. We tested the hypothesis that insects are regularly exposed to infections or invasions in nature and here report results of a field study designed to assess the extent of natural infections in insects collected from agrarian fields surrounding Kahramanmaraş, Turkey. Specimens were dissected to assess numbers of nodules. Formation of darkened, melanotic nodules is the predominant cellular immune reaction to microbial and parasitic infection, and once formed, the nodules are permanently attached to internal surfaces. The collected insects were healthy. Of the >400 examined specimens, at least some nodules were found in 98%. Numbers of nodules ranged from approximately 2/individual to >100 nodules/individual. We conclude that insects are regularly challenged by microbial and parasitic infections from which they recover. The novel implication of our data is that insect immune systems may limit the host range and effectiveness of agents deployed in biological control programs. Knowledge of insect immune systems may contribute to increased use of biopesticides globally.

The entomopathogenic bacterium, Xenorhabdus nematophila, induces immunodepression in target insects and finally leads to lethal septicemia of the infected hosts. A hypothesis has been raised that the bacteria inhibit eicosanoid-biosynthesis pathway to interrupt immune signaling of the infected hosts. Here, we show direct evidence that X. nematophila inhibits the activity of phospholipase A2 (PLA2), the initial step in the eicosanoid-biosynthesis pathway. Inhibition of PLA2 was dependent on both incubation time with X. nematophila and the bacterial concentration in in vitro PLA2 preparations of Manduca sexta hemocytes. While living bacteria inhibited PLA2 activity, heat-killed X. nematophila rather increased PLA2 activity. X. nematophila secreted PLA2 inhibitor(s), which were detected in the organic, but not aqueous, extract of the bacterial culture medium. The PLA2 inhibitory activity of the organic extract was lost after heat treatment. These results clearly indicate that X. nematophila inhibits PLA2 activity and thereby inhibits eicosanoid biosynthesis, which leads to immunodepression of the infected hosts.