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      Interleukin-12 protects mice against disseminated infection caused by Paracoccidioides brasiliensis but enhances pulmonary inflammation.

      Clinical Immunology (Orlando, Fla.)
      Animals, Antibodies, Fungal, biosynthesis, Cytokines, Disease Models, Animal, Humans, Hypersensitivity, Delayed, Immunotherapy, Interleukin-12, pharmacology, Leukocytes, Mononuclear, immunology, pathology, Lung, microbiology, Male, Mice, Paracoccidioides, isolation & purification, Paracoccidioidomycosis, etiology, prevention & control

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          Abstract

          Paracoccidioides brasiliensis is a facultative, intracellular pathogen causing the most important deep mycosis in Latin America. As the production of IFN-gamma and induction of cell-mediated immunity to P. brasiliensis is of critical importance in host defense, the immunotherapeutic effect of exogenous IL-12 administration was studied in a murine model of susceptibility to pulmonary infection. rIL-12 treatment led to a less disseminated disease, as confirmed by decreased fungal loads in liver and spleen. Administration of rIL-12 did not affect fungal growth in the lungs, although it did induce an augmented pulmonary mononuclear cell inflammation. IL-12 treatment induced an early (week 1) increase in pulmonary IFN-gamma, but decreased cytokine and specific antibody (IgG1 and IgG3) production at week 8 after infection. These results show that IL-12 administration induces a less severe infection, but the high inflammatory response detected in the lungs precludes its possible use as a new therapeutic tool for severe paracoccidioidomycosis. (c) 2002 Elsevier Science (USA).

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