The primary aim of this study was to analyse the influence of honeybee venom on various aspects of Drosophila melanogaster physiology and to assess the efficacy of adipokinetic hormone (AKH) in mitigating venom toxicity. We examined the harmful effects of venom on the thoracic muscles and central nervous system of Drosophila, as well as the potential use of AKH to counteract these effects. The results demonstrated that envenomation altered AKH levels in the Drosophila CNS, promoted cell metabolism, as evidenced by an increase in citrate synthase activity in muscles, and improved relative cell viability in both organs incubated in vitro. Furthermore, venom treatment reduced the activity of two key antioxidative stress enzymes, superoxide dismutase and catalase, and modified the expression of six genes encoding immune system components (Keap1, Relish, Nox, Eiger, Gadd45, and Domeless) in both organs. The venom also disrupted muscle cell ultrastructure, specifically myofibrils, and increased the release of arginine kinase into the incubation medium. Notably, when administered alongside the venom, AKH influenced the majority of these changes. AKH was the most effective in minimising damage to the ultrastructure of muscle cells and preventing the release of arginine kinase from muscles to the medium; however, in other parameters, the effect was modest or minimal. Given that honeybee venom often affects humans, understanding its actions and potential ways to reduce or eliminate them is valuable and could lead to the development of pharmacologically important compounds that may have clinical relevance.

• Keywords
• Adipokinetic hormone, Arginine kinase, Bee venom, Drosophila model, Immune responsible genes, Muscle structure,
• MeSH
• Central Nervous System drug effects   metabolism   MeSH
• Drosophila melanogaster drug effects   metabolism   MeSH
• Insect Hormones * pharmacology   metabolism   MeSH
• Pyrrolidonecarboxylic Acid * analogs & derivatives   pharmacology   metabolism   MeSH
• Oligopeptides * pharmacology   metabolism   MeSH
• Bee Venoms * toxicity   antagonists & inhibitors   MeSH
• Bees MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH
• Names of Substances
• adipokinetic hormone MeSH Browser
• Insect Hormones * MeSH
• Pyrrolidonecarboxylic Acid * MeSH
• Oligopeptides * MeSH
• Bee Venoms * MeSH

Insect adipokinetic hormones (AKHs) are neuropeptides with a wide range of actions, including the control of insect energy metabolism. These hormones are also known to be involved in the insect defence system against toxins and pathogens. In this study, our aim was to demonstrate whether the application of external AKHs significantly enhances the efficacy of the entomopathogenic fungus Isaria fumosorosea in a model species (firebug Pyrrhocoris apterus) and pest species (Egyptian cotton leafworm Spodoptera littoralis and pea aphid Acyrthosiphon pisum). It was found that the co-application of Isaria with AKHs significantly enhanced insect mortality in comparison to the application of Isaria alone. The mode of action probably involves an increase in metabolism that is caused by AKHs (evidenced by the production of carbon dioxide), which accelerates the turnover of Isaria toxins produced into the infected insects. However, several species-specific differences probably exist. Intoxication by Isaria elicited the stimulation of Akh gene expression and synthesis of AKHs. Therefore, all interactions between Isaria and AKH actions as well as their impact on insect physiology from a theoretical and practical point of view need to be discussed further.

• Keywords
• AKH, carbon dioxide production, entomopathogen, insect pest, metabolism, mortality,
• Publication type
• Journal Article MeSH

Entomopathogenic nematodes (EPNs) are efficient insect parasites, that are known for their mutualistic relationship with entomopathogenic bacteria and their use in biocontrol. EPNs produce bioactive molecules referred to as excreted/secreted products (ESPs), which have come to the forefront in recent years because of their role in the process of host invasion and the modulation of its immune response. In the present study, we confirmed the production of ESPs in the EPN Heterorhabditis bacteriophora, and investigated their role in the modulation of the phenoloxidase cascade, one of the key components of the insect immune system. ESPs were isolated from 14- and 21-day-old infective juveniles of H. bacteriophora, which were found to be more virulent than newly emerged nematodes, as was confirmed by mortality assays using Galleria mellonella larvae. The isolated ESPs were further purified and screened for the phenoloxidase-inhibiting activity. In these products, a 38 kDa fraction of peptides was identified as the main candidate source of phenoloxidase-inhibiting compounds. This fraction was further analyzed by mass spectrometry and the de novo sequencing approach. Six peptide sequences were identified in this active ESP fraction, including proteins involved in ubiquitination and the regulation of a Toll pathway, for which a role in the regulation of insect immune response has been proposed in previous studies.

• Keywords
• Galleria mellonella, Heterorhabditis bacteriophora, excreted/secreted products, immunity, melanization, phenoloxidase, virulence,
• Publication type
• Journal Article MeSH

The pathogenic effect of mutant HTT (mHTT) which causes Huntington disease (HD) are not restricted to nervous system. Such phenotypes include aberrant immune responses observed in the HD models. However, it is still unclear how this immune dysregulation influences the innate immune response against pathogenic infection. In the present study, we used transgenic Drosophila melanogaster expressing mutant HTT protein (mHTT) with hemocyte-specific drivers and examined the immune responses and hemocyte function. We found that mHTT expression in the hemocytes did not affect fly viability, but the numbers of circulating hemocytes were significantly decreased. Consequently, we observed that the expression of mHTT in the hemocytes compromised the immune responses including clot formation and encapsulation which lead to the increased susceptibility to entomopathogenic nematode and parasitoid wasp infections. In addition, mHTT expression in Drosophila macrophage-like S2 cells in vitro reduced ATP levels, phagocytic activity and the induction of antimicrobial peptides. Further effects observed in mHTT-expressing cells included the altered production of cytokines and activation of JAK/STAT signaling. The present study shows that the expression of mHTT in Drosophila hemocytes causes deficient cellular and humoral immune responses against invading pathogens. Our findings provide the insight into the pathogenic effects of mHTT in the immune cells.

• Keywords
• Drosophila melanogaster, Huntington's disease, antimicrobial peptide (AMPs), cytokines, immunity, infection, phagocytosis,
• MeSH
• Cell Line MeSH
• Drosophila melanogaster MeSH
• Gene Expression * MeSH
• Animals, Genetically Modified MeSH
• Hemocytes immunology   MeSH
• Immunity, Humoral * MeSH
• Humans MeSH
• Huntingtin Protein genetics   immunology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• HTT protein, human MeSH Browser
• Huntingtin Protein MeSH