Location: Biological Control of Insects ResearchTitle: Nitric oxide mediates insect cellular immunity via phospholipase A2 activation Author
Submitted to: Journal of Innate Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/18/2017
Publication Date: N/A
Citation: N/A Interpretive Summary: Chemical insecticides are effective pest insect management tools, however, negative effects, including environmental contamination and insect resistance to the insecticides attend use of these products. These negative effects drive research into alternative insect management technologies such as biological control based on deploying insect pathogenic microbes, known as microbial control. The problem with microbial insect control is insects have very powerful immune responses to pathogenic microbes, which reduces the efficacy of these microbes. We address this problem with research designed to understand and limit insect immunity. In this paper we report on how insects signal their immune responses to microbial infections. We identified two separate immune signals that operate together to produce coordinated, controlled reactions to infections. The coordination represents new, researchable targets that may be exploited to increase the effectiveness of microbial biological controls of insect pests. This new finding will be used by scientists working to suppress insect immune systems and will ultimately benefit growers and consumers of vegetable and other food crops.
Technical Abstract: After infection or invasion is recognized, biochemical mediators act in signaling insect immune functions. These include biogenic amines, insect cytokines, eicosanoids and nitric oxide (NO). Treating insects or isolated hemocyte populations with different mediators often leads to similar results. Separate treatments with an insect cytokine, two biogenic amines and an eicosanoid lead to a single result, hemocyte spreading, understood in terms of intracellular cross-talk among these signaling systems. This study focuses on cross-talk between NO and eicosanoid signaling in our model insect, Spodoptera exigua. Bacterial injection increased NO concentrations in larval hemocytes and fat body and RNA interference (RNAi) of SeNOS suppressed NO concentrations. RNAi-treatment also led to a significant reduction in hemocyte nodulation following bacterial injection. Similar RNAi treatments led to significantly reduced PLA2 activities in hemocytes and fat body compared to control larvae. Injection of L-NAME also prevented the induction of PLA2 activity following bacterial challenge. An injected NO donor, S-nitroso-N-acetyl-DL-penicillamine, increased PLA2 activity in a dose-dependent manner. However, eicosanoids did not influence NO concentrations in immune challenged larvae. We infer that NO and eicosanoid signaling operate via cross-talk mechanisms in which the elevated NO concentrations activate PLA2 and eicosanoid biosynthesis, which finally mediates various immune responses.