Poster 49 - Evaluation of immune response induced in mice by Thalassophryne nattereri fish venom

Poster 49. Congresso da Sociedade Brasileira de Toxinologia, 8., Symposium of the Pan American Section of the International Society on Toxinology, 8., 2004, Angra dos Reis, Brasil. Abstracts... J. Venom. Anim. Toxins incl.Trop. Dis., 2004, 10, 3, p.408.

Evaluation of immune response induced in mice by Thalassophryne nattereri fish venom

¹Grund,L.Z.; ¹Piran-Soares, A.A.; ²Souza, V.M.O.; ³Lima,C.; ¹Lopes-Ferreira, M.;

1 Laboratório de Imunopatologia, Instituto Butantan, 2 Departamento de Imunologia, Universidade de São Paulo, 3 Departamento de Farmacologia, Universidade de São Paulo, São Paulo.

The Thalassophryne nattereri venomous fish (niquim) is responsible for many accidents in fishermen and swimmers in the northeast of Brazil and the envenomation provoked by this fish produce an important economic, medical and social problem in this country. The accidents are characterized by local effect with intense pain, edema, erythema and necrosis. The objective of this work was to evaluate the profile of the immune response developed after injection of mice with T. nattereri venom. We analyzed the serum levels of IgM and IgG antibodies and the profile of cytokines produced by spleen cells after the restimulation in vitro. Balb/c mice were immunized at days 0 and 7 with 10 mg of venom adsorbed in 1,6 mg of Al(OH)3. Animals immunized only with Al(OH)3 were considered as control-group. The animals were bled at days –1, 7 and 14, and venom-specific IgG1 and IgG2a antibody levels were determined by ELISA. Fourteen days after the first immunization, animals were sacrificed to obtain the spleen, and then cellular suspension was restimulated with venom (10 mg) or Concanavalina A –Con A (5 mg). Our findings show that immunization with T. nattereri venom induced moderate levels of venom-specific IgM and IgG in the primary response. On the other hand, the venom induced a marked increase in IgG antibodies in secondary response, mainly on IgG1 and IgG2a subclasses. Furthermore, we observed a spontaneous production of IFN-g and IL-5 by non-stimulated spleenic cells. Interestingly, spleen cells restimulated with venom exhibited higher levels of IFN-g and an augmentation of fivefold in the IL-5 levels. When the cells were restimulated with Con A the venom diminished twofold the synthesis of IL-4. In conclusion, these results suggest that high level of IgG1 and IgG2a induced by T. nattereri venom can be related with the profile of cytokine induced by venom (IFN-g and IL-5). Additionally, the inhibition of the IL-4 synthesis by the venom correlated with marked levels of IFN-g. Finally, we suggest that T. nattereri venom can induce the development of both types of lymphocytes Th1 and Th2.