Abstract
We hypothesized that beyond the Thalassophryne nattereri venoms ability to induce in mice a strong specific-Th2 response with high levels of specific IgE/IgG1, it would be able to trigger anaphylaxis in sensitized individuals. To investigate whether the venom is capable of inducing an allergic reaction in mice and characterize soluble and cellular mediators involved in this process, BALB/c female mice were sensitized intraperitoneally with decreasing-dose of venom at weekly intervals for 4 weeks and challenged by intraperitoneal, oral or epicutaneous routes with venom 2 weeks later. Our data show that sensitized-mice challenged by all routes showed intense symptoms of anaphylaxis, dependent on the anaphylactic IgG1 and IgE antibodies and mast cells. The late-phase reaction developed after initial symptoms was characterized by the influx of eosinophils, dependent on IL-5, IL-17A and eotaxin produced by Th2 cells in inflamed lungs and skin draining lymph-nodes. Using C57BL/6 deficient mice we demonstrated that IL-4 KO mice failed to develop anaphylactic symptoms or local Th2 inflammation, producing low levels of IgG1 and increased levels of IgG2a. Together our results demonstrated that the venom of T. nattereri has allergenic proteins that can trigger an allergic process, a phenomenon IgE-IgG1 dependent, IL-4-mediated and negatively regulated by IFN-γ.
Highlights
Few studies have explored the mechanisms underlying allergy disorders triggered by venom from marine/aquatic organisms, other than the study that identified the venoms of anemone and jellyfish from the phylum Cnidaria as causing anaphylaxis in humans[1]
We hypothesized that the toxins of T. nattereri venom immunogenic would be capable of inducing an allergic process, characterized as chronic and Th2 mediated
Together our results show that the sensitized-mice with decreasing dose of venom developed: a) anaphylaxis with scores ranging from mild to severe, depending on challenge routes; b) produced anaphylactic IgG1 and IgE Abs; c) showed Natterins-specific IgG in the sera; d) recruited eosinophils and neutrophils to the lungs and to the skin later after decay of symptoms
Summary
Few studies have explored the mechanisms underlying allergy disorders triggered by venom from marine/aquatic organisms, other than the study that identified the venoms of anemone and jellyfish from the phylum Cnidaria as causing anaphylaxis in humans[1]. Fish of toxicological importance are grouped into the venomous category, which present glands specialized in the secretion of venom and a specialized apparatus (spines with canals or canaliculated) for its inoculation[2]. The venom apparatus of T. nattereri is composed of two dorsal and two lateral canaliculated spines covered by a membrane connected to venom glands at the base of the fins (Fig. 1B). Lopes-Ferreira et al.[11] evidenced that low dose of venom (0.3 μg/mice), in injured tissue of mice, lead to an intense vascular congestion, stasis of blood flow in postcapillary venules and capillaries, beyond focal transient constrictions in arterioles. Low numbers of phagocytic cells during the first 24 h after VTn injection and the presence of necrotic material which had not been cleared out seven days after envenomation were described www.nature.com/scientificreports in injured tissues[12]. We observed a delayed influx of neutrophils to the injured site of venom-injected mice, arriving only after 24 h13
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