Do Código Florestal para o Código da Biodiversidade

Em face do gigantismo do território e da situação real em que se encontram os seus macro biomas - Amazônia Brasileira, Brasil Tropical Atlântico, Cerrados do Brasil Central, Planalto das Araucárias, e Pradarias Mistas do Brasil Subtropical - e de seus numerosos mini-biomas, faixas de transição e relictos de ecossistemas, qualquer tentativa de mudança no "Código Florestal" tem que ser conduzido por pessoas competentes e bioeticamente sensíveis. Por muitas razões, se houvesse um movimento para aprimorar o atual Código Florestal, teria que envolver o sentido mais amplo de um Código de Biodiversidades, levando em conta o complexo mosaico vegetacional de nosso território. Enquanto o mundo inteiro trabalha para a diminuição radical de emissão de CO2, o projeto de reforma proposto na Câmara Federal de revisão do Código Florestal defende um processo que significará uma onda de desmatamento e emissões incontroláveis de gás carbônico, fato observado por muitos críticos em diversos trabalhos e entrevistas. A utopia de um desenvolvimento com o máximo de florestas em pé não pode ser eliminada por princípio em função de mudanças radicais do Código Florestal, sendo necessário pensar no território total de nosso país, sob um ampliado e correto Código de Biodiversidade. Ou seja, um pensamento que envolva: as nossas grandes florestas (Amazônia e Matas Tropicais Atlânticas); o domínio das caatingas e agrestes sertanejos; planaltos centrais com cerrados, cerradões e campestres; os planaltos de araucárias sul-brasileiros; as pradarias mistas do Rio Grande do Sul; e os redutos e mini-biomas da costa brasileira e do Pantanal mato-grossense, e faixas de transição e contrato (core-áreas) de todos os domínios morfoclimáticos e fitogeográficos brasileiros).

PAS-1, an Ascaris suum Protein, Modulates Allergic Airway Inflammation via CD8(+) gamma delta TCR(+) and CD4(+) CD25(+) FoxP3(+) T Cells

We have previously demonstrated that PAS-1, a 200 kDa protein from Ascaris suum, has a potent immunomodulatory effect on humoral and cell-mediated responses induced by APAS-3 (an allergenic protein from A. suum) or unrelated antigens. In this study, we investigated the mechanisms by which PAS-1 is able to induce this effect on an allergic airway inflammation induced by OVA in mice. C57BL/6 mice were adoptively transferred on day 0 with seven different PAS-1-primed cell populations: PAS-1-primed CD19(+) or B220(+) or CD3(+) or CD4(+) or CD8(+) or CD4(+) CD25) or CD4(+) CD25(+) lymphocytes. These mice were immunized twice with OVA and alum by intraperitoneal route (days 0 and 7) and challenged twice by intranasal route (days 14 and 21). Two days after the last challenge, the airway inflammation was evaluated by antibody levels, cellular migration, eosinophil peroxidase levels, cytokine and eotaxin production, and pulmonary mechanical parameters. Among the adoptively transferred primed lymphocytes, only CD4(+) CD25(+), CD8(+) or the combination of both T cells impaired the production of total IgE and OVA-specific IgE and IgG1 antibodies, eosinophilic airway inflammation, Th2-type cytokines (IL-4, IL-5 and IL-13), eotaxin release and airway hyperreactivity. Moreover, airway recruited cells from CD4(+) CD25(+) and CD8(+) T-cell recipient secreted more IL-10/TGF-beta and IFN-gamma, respectively. Moreover, we found that PAS-1 expands significantly the number of CD4(+) CD25(+) FoxP3(+) and CD8(+) gamma delta TCR(+) cells. In conclusion, these findings demonstrate that the immunomodulatory effect of PAS-1 is mediated by these T-cell subsets.

PAS-1, a protein from Ascaris suum, modulates allergic inflammation via IL-10 and IFN-gamma, but not IL-12

Helminths and their products have a profound immunomodulatory effect upon the inductive and effector phases of inflammatory responses, including allergy. We have demonstrated that PAS-1, a protein isolated from Ascaris strum worms, has an inhibitory effect on lung allergic inflammation due to its ability to down-regulate eosinophilic inflammation, Th2 cytokine release and IgE antibody production. Here, we investigated the role of IL-12, IFN-gamma and IL-10 in the PAS-1-induced inhibitory mechanism using a murine model of asthma. Wild type C57BL/6, IL-12(-/-), IFN-gamma(-/-) and IL-10(-/-) mice were immunized with PAS-1 and/or OVA and challenged with the same antigens intranasally. The suppressive effect of PAS-I was demonstrated on the cellular influx into airways, with reduction of eosinophil number and eosinophil peroxidase activity in OVA + PAS-1-immunized wild type mice. This effect well correlated with a significant reduction in the levels of IL-4, IL-5, IL-13 and eotaxin in BAL fluid. Levels of IgE and IgG1 antibodies were also impaired in serum from these mice. The inhibitory activity of PAS-I was also observed in IL-12(-/-) mice, but not in IFN-gamma(-/-) and IL-10(-/-) animals. These data show that IFN-gamma and IL-10, but not IL-12, play an important role in the PAS-1 modulatory effect. (C) 2008 Elsevier Ltd. All rights reserved.