Immune factors and immunoregulation in tuberculosis

Pathogens causing tuberculosis and other chronic infectious diseases of major public health importance commonly have complex mechanisms involved in their persistence in the host despite specific and sometimes strong immune responses. These diseases are also associated with the lack of efficient vaccines, difficult therapeutics and a high mortality rate among susceptible individuals. Here, we will review features of the host immune response that contribute to the occurrence of disease. In addition, we propose that the immune responses observed in tuberculosis cannot be interpreted solely on the basis of a Th1-Th2 counter-regulatory paradigm since there is growing evidence that natural regulatory T cells may play an important role in the regulation of host immune responses against Mycobacterium tuberculosis. Thus, the development of more effective vaccines against this bacterial disease should take into account the role of natural regulatory T cells in the progression to severe disease and persistence of infection. Finally, new treatments based on manipulation of regulatory T cells should be investigated.

Efeitos de imunopotenciadores nao especificos na infeccao experimental pelo Schistosoma mansoni. I. Levamisole / Effects of non-specific immunopotentiators in experimental Schistosoma mansoni infection. I. Levamisole

Os efeitos do levamisole nas alteracoes histopatologicas, resistencia do hospedeiro e quimiotaxia "in vitro" foram estudados na infeccao experimental pelo Schistosoma mansoni em camundongos da linhagem C57B1/10. O tratamento profilatico resultou em um aumento no numero de vermes adultos obtidos pela perfusao e tambem em uma taxa de mortalidade maior (p<0,05). As alteracoes histopatologicas (figado e intestino) foram similares em todos os grupos. Uma reducao significante da quimiotaxia "in vitro" ocorreu em camundongos controles infectados, assim como naqueles submetidos a tratamento profilatico com levamisole. A atividade quimiotatica atingiu os mesmos niveis dos camundongos controles normais (nao-infectados e nao-tratados com levamisole), quando o esquema curativo foi usado. O levamisole parece aumentar a susceptibilidade de camundongos da linhagem C57B1/10 a infeccao pelo S. mansoni quando administrado antes da infeccao e normaliza a atividade quimiotatica, quando dado apos a infeccao.

Immunochemical localization of the fraction-1 antigen, a virulence determinant of Yersinia pestis

The distribution of Yersina pestis Fraction-1 (F1) antigen was analyzed in cells grown at 28§C and 37§C. Fractionation of Y. pestis cells followed by analysis in SDS-polyacrylamide gel electrophoresis indicated that the mature form of the F1 antigen is localized in the extracellular matrix and in the cytoplasm. Localization of the F1 antigen was confirmed by immunoblots and a single peptide with a molecular weight of 17,000 daltons was recognized. Electron microscopy of Y. pestis cells labeled with colloidal gold-conjugated antibodies corroborated the extracellular matrix and cytoplasm dual location of the F1 antigen

Comparative studies of Yersinia pestis outer membrane isolation techniques and their potential use in plague epidemiology

No presente estudo tres tecnicas para isolamento de fracoes enriquecidas em membrana externa de Y. pestis foram avaliadas. As tecnicas utilizadas foram: centrifugacao em gradiente de densidade em sacarose e solubilizacao diferencial com Sarkosyl ou Triton X-100. A analise por eletroforese em gel de poliacrilamida na presenca de dodecil sulfato de sodio (SDS-PAGE) das membranas externas extraidas pelos diferentes metodos evidenciou perfis proteicos semelhantes. A determinacao das atividades de NADH-desidrogenase e succinato-desidrogenase (enzimas de membrana interna) indicou que todas as preparacoes estudadas eram adequadas a estudos analiticos. Obteve-se evidencias preliminares sobre o possivel uso de perfis proteicos de membrana externa na identificacao de variantes geograficos entre isolados selvagens de Y. pestis

In vivo leukocyte chemotaxis during the development of acute experimental Trypanosoma cruzi infection

Five and 15 days after T. cruzi infection, staphylococcal protein A was injected into a connective tissue air pouch of mice and the migration of polymorphonuclear leukocyrtes into the area was monitored. The PMN leukocyte response of 15-day infected mice was lower than of uninfected mice (P < 0.001): The 15 - day infected mice also showed a lower leukocyte response when compared to 5 - day infected mice (P < 0.001). These data suggest that chemotaxis defect development gradually during the acute phase of infection