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A thorough history and physical is essential to the evaluation of this condition and to help in distinguishing it from mimics. Although microscopic identification of nematocyst cnidocytes from skin scrapings has been successfully performed in studies,[21] most institutions will likely lack the personnel capable of identifying these structures, and widely available commercial testing in this manner has not been established. There is no commercially available specific laboratory test to confirm the presence of Irukandji syndrome or the sting of Irukandji-causing jellyfish. As such, the diagnosis is made clinically.

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As the sister group to bilaterians, cnidarians stand in a unique phylogenetic position that provides insight into evolutionary aspects of animal development, physiology, and behavior. While cnidarians are classified into two types, sessile polyps and free-swimming medusae, most studies at the cellular and molecular levels have been conducted on representative polyp-type cnidarians and have focused on establishing techniques of genetic manipulation. Recently, gene knockdown by delivery of short hairpin RNAs into eggs via electroporation has been introduced in two polyp-type cnidarians, Nematostella vectensis and Hydractinia symbiolongicarpus, enabling systematic loss-of-function experiments. By contrast, current methods of genetic manipulation for most medusa-type cnidarians, or jellyfish, are quite limited, except for Clytia hemisphaerica, and reliable techniques are required to interrogate function of specific genes in different jellyfish species. Here, we present a method to knock down target genes by delivering small interfering RNA (siRNA) into fertilized eggs via electroporation, using the hydrozoan jellyfish, Clytia hemisphaerica and Cladonema paciificum. We show that siRNAs targeting endogenous GFP1 and Wnt3 in Clytia efficiently knock down gene expression and result in known planula phenotypes: loss of green fluorescence and defects in axial patterning, respectively. We also successfully knock down endogenous Wnt3 in Cladonema by siRNA electroporation, which circumvents the technical difficulty of microinjecting small eggs. Wnt3 knockdown in Cladonema causes gene expression changes in axial markers, suggesting a conserved Wnt/β-catenin-mediated pathway that controls axial polarity during embryogenesis. Our gene-targeting siRNA electroporation method is applicable to other animals, including and beyond jellyfish species, and will facilitate the investigation and understanding of myriad aspects of animal development.

Abstract:Jellyfish venom is well known for its local skin toxicities and various lethal accidents. The main symptoms of local jellyfish envenomation include skin lesions, burning, prickling, stinging pain, red, brown, or purplish tracks on the skin, itching, and swelling, leading to dermonecrosis and scar formation. However, the molecular mechanism behind the action of jellyfish venom on human skin cells is rarely understood. In the present study, we have treated the human HaCaT keratinocyte with Nemopilema nomurai jellyfish venom (NnV) to study detailed mechanisms of actions behind the skin symptoms after jellyfish envenomation. Using two-dimensional gel electrophoresis (2-DE) and matrix-assisted laser desorption-ionization time-of-flight mass spectrometry (MALDI-TOF/MS), cellular changes at proteome level were examined. The treatment of NnV resulted in the decrease of HaCaT cell viability in a concentration-dependent manner. Using NnV (at IC50), the proteome level alterations were determined at 12 h and 24 h after the venom treatment. Briefly, 70 protein spots with significant quantitative changes were picked from the gels for MALDI-TOF/MS. In total, 44 differentially abundant proteins were successfully identified, among which 19 proteins were increased, whereas 25 proteins were decreased in the abundance levels comparing with their respective control spots. DAPs involved in cell survival and development (e.g., Plasminogen, Vinculin, EMILIN-1, Basonuclin2, Focal adhesion kinase 1, FAM83B, Peroxisome proliferator-activated receptor-gamma co-activator 1-alpha) decreased their expression, whereas stress or immune response-related proteins (e.g., Toll-like receptor 4, Aminopeptidase N, MKL/Myocardin-like protein 1, hypoxia up-regulated protein 1, Heat shock protein 105 kDa, Ephrin type-A receptor 1, with some protease (or peptidase) enzymes) were up-regulated. In conclusion, the present findings may exhibit some possible key players during skin damage and suggest therapeutic strategies for preventing jellyfish envenomation.Keywords: Nemopilema nomurai jellyfish; 2-DE; MALDI-TOF/MS; HaCaT cell; dermal toxicityKey Contribution: This is the first report revealing the dermal molecular changes at proteomic level induced by jellyfish venom, which may lead us to understand the pathogenesis and hopefully suggest an idea of interrupting the dermal poisoning symptoms.

Although this study demonstrates the anticancer effect of NnV, identifying the molecular mechanisms associated with this activity is difficult because full identification and characterization of individual components of venom have not been done. A previous study and unpublished proteomic data (being prepared for publication) demonstrated that NnV contains an abundant amount of metalloprotease-like enzymes [16]. According to proteomic profile, 150 toxin proteins were identified by 2-DE, including metalloprotease, serine protease inhibitor, phospholipase, and serine protease. Metalloproteases were major component in the N. nomurai venom with a proportion of 21% of the identified venom toxins. In other venoms (snakes and spiders), metalloprotease exerted inhibitory effects on cancer cell adhesion, proliferation, migration, invasion, and angiogenesis. Several studies reported that venom metalloprotease has potential anticancer effects [44]. The extracellular matrix (ECM) plays important roles in cell behavior and function, including growth, death, adhesion, and migration. These changes are mainly involved with interaction of integrin receptors, which can lead to apoptosis in cancer cells. Anoikis, a special type of apoptosis, is provoked by degradation of ECM components such as matrix metalloproteinases (MMP) [45]. Jararhagin, a purified snake venom metalloprotease from Bothrops jararaca, exhibited an inhibitory effect on cell adhesion and a cytotoxic effect on melanoma cells [46, 47]. TSV-DM, a metalloprotease from Trimeresurus stejnegeri, brought about inhibition of cell proliferation and induction of apoptotic cell death in ECV304 cells [48]. To investigate whether the anticancer effect of NnV is associated with metalloprotease, cell viability was assessed after preincubation with NnV and MMP inhibitors (tetracycline). NnV treatment alone caused 50% cytotoxicity in HepG2 cells, while cotreatment between NnV and Tetra had little effect on cell viability. Next, we tried to isolate the bioactive component that exerts the anticancer effect. We obtained three peaks, and each fraction was assessed for cytotoxicity in HepG2 cells. Compared with crude venom (NnV), F1 and F2 induced similar cytotoxicity, while NnV-F3 induced less cytotoxicity. To identify and characterize the active components that have an anticancer effect, sufficient amounts of NnV-F1 and NnV-F2 are necessary. However, NnV-F1 and NnV-F2 had very low protein concentrations, making it difficult to identify and characterize the active components. Other groups reported that identification of individual components of jellyfish venom is very difficult as a large amount of venom is necessary for isolation and characterization, and the venom has unstable properties and an insufficient amount of previously published data, unlike other types of venom (snake and scorpion) [17, 49]. Despite the potential of NnV, obtaining sufficient amounts of venom for further studies for identification and characterization remains a significant challenge.