Abstract:Injecting the insect pathogenic bacterium Photorhabdus luminescens into the blood system of the model lepidopteran insect Manduca sexta induces nitric oxide synthase (NOS) expression in the fat body and blood cells (haemocytes), whereas following oral ingestion of bacteria NOS expression is limited to the gut. We used RNA interference to knock-down expression of NOS throughout the insect. Preventing NOS induction in this way adversely affected the survival of orally infected insects and caused a significant in… Show more
“…Bacterial challenge significantly increased SeNOS expression, indicating that SeNOS is an iNOS, as seen in other lepidopterans, including M. sexta [18] and B. mori [19].…”
Section: Discussionmentioning
confidence: 91%
“…More to the point, the inducible expression of NOS is site-specific to the foci of pathogen infection in M. sexta. Eleftherianos et al [18] demonstrated this by infecting hornworms with a bacterial pathogen, Photorhabdus luminescens, at different sites. M. sexta expressed NOS only in gut tissue following oral infection and only in the fat body and hemocytes following infection by hemocelic injection.…”
Section: Discussionmentioning
confidence: 99%
“…NO also induces both cellular and humoral immune responses via the Toll/IMD signal pathways in Drosophila [16,17]. Regulation of NOS expression is directly associated with the immune response in Manduca sexta [18]. An ENF-family cytokine that triggers AMP gene expression elevates NO concentration in Bombyx mori by inducing NOS expression, suggesting a cross-talk mechanism between cytokine and NO signaling in insects [19].…”
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, 2 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 the cross-talk between NO and eicosanoid signaling in our model insect, Spodoptera exigua. Bacterial injection increased NO concentrations in the larval hemocytes and fat body, and RNA interference (RNAi) of the S. exigua NO synthase (NOS) gene 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 the 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.
“…Bacterial challenge significantly increased SeNOS expression, indicating that SeNOS is an iNOS, as seen in other lepidopterans, including M. sexta [18] and B. mori [19].…”
Section: Discussionmentioning
confidence: 91%
“…More to the point, the inducible expression of NOS is site-specific to the foci of pathogen infection in M. sexta. Eleftherianos et al [18] demonstrated this by infecting hornworms with a bacterial pathogen, Photorhabdus luminescens, at different sites. M. sexta expressed NOS only in gut tissue following oral infection and only in the fat body and hemocytes following infection by hemocelic injection.…”
Section: Discussionmentioning
confidence: 99%
“…NO also induces both cellular and humoral immune responses via the Toll/IMD signal pathways in Drosophila [16,17]. Regulation of NOS expression is directly associated with the immune response in Manduca sexta [18]. An ENF-family cytokine that triggers AMP gene expression elevates NO concentration in Bombyx mori by inducing NOS expression, suggesting a cross-talk mechanism between cytokine and NO signaling in insects [19].…”
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, 2 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 the cross-talk between NO and eicosanoid signaling in our model insect, Spodoptera exigua. Bacterial injection increased NO concentrations in the larval hemocytes and fat body, and RNA interference (RNAi) of the S. exigua NO synthase (NOS) gene 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 the 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.
“…It was suggested that although NO signalling emanates from a tissue other than blood cells it needs the latter to exercise its effect in the fat body (Djikers and O'Farrell, 2007). The guts of insects release NO (Foley and O'Farell, 2003;Eleftherianos et al, 2009), and following oral infection of Drosophila larvae with Ecc the gut is the tissue where bacteria activate dipt-GFP prior to fat-body expression and a systemic Journal of Cell Science 122 (24) Fig. 7.…”
In Drosophila, the humoral response characterised by the synthesis of antimicrobial peptides (AMPs) in the fat body (the equivalent of the mammalian liver) and the cellular response mediated by haemocytes (blood cells) engaged in phagocytosis represent two major reactions that counter pathogens. Although considerable analysis has permitted the elucidation of mechanisms pertaining to the two responses individually, the mechanism of their coordination has been unclear. To characterise the signals with which infection might be communicated between blood cells and fat body, we ablated circulating haemocytes and defined the parameters of AMP gene activation in larvae. We found that targeted ablation of blood cells influenced the levels of AMP gene expression in the fat body following both septic injury and oral infection. Expression of the AMP gene drosomycin (a Toll target) was blocked when expression of the Toll ligand Spätzle was knocked down in haemocytes. These results show that in larvae, integration of the two responses in a systemic reaction depend on the production of a cytokine (spz), a process that strongly parallels the mammalian immune response.
“…NOS (accession number (AN): AF062749) is induced in the midgut of Manduca sexta larvae fed with Photorhabdus luminescens. If the expression of NOS is knocked-down the survival of orally infected insects is affected and a significant increase in the number of bacteria crossing into the haemolymph was observed [6]. In Bombyx mori NOS is induced in the fat body by lipopolysaccharides [11].…”
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