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Efeito do Mycobacterium bovis BCG, lipopolissacarideo bacteriano e hidrocortisona no desenvolvimento de imunidade ao Plasmodium berghei em camundongos

Effects of mycobacterium bovis BCG, bacterial lipopolysaccharide and hydrocortisone on the development of immunity to Plasmodium berghei

Resumos

Mycobacterium bovis (BCG) aumenta significantemente o desenvolvimento da imunidade nos camundongos CFW, C57BL/6, C57BL/l0ScN e BALB/c (Nu/+) para os estágios eritrocitos do Plasmodium berghei. Camundongos tratados com BCG requerem menos ciclos de infecção com P. berghei e cura pelo Fansidar (pirimetamina + sulfadoxina) para desenvolverem imunidade sólida a este parasita do que os controles. Contudo, os animais que receberam BCG 30 dias antes do início da imunização evidenciaram uma perda precoce da imunidade adquirida para o P. berghei, quando comparado com os animais que receberam BCG 14 dias antes ou que não receberam BCG. Assim, sendo, o BCG aumentada a indução na resposta imune do hospedeiro ao P. berghei no curso de infecções subseqüentes. O tratamento de camundongos CFW, BALB/c e C57BL/6 com lipopolissacarídeo bacteriano ou hidrocortisona faz com que os animais requeiram um número maior de ciclos de infecção e cura para tornarem-se imunes ao P. berghei que os controles. O tratamento dos camundongos C57BL/10ScN com hidrocortisona aboliu completamente a sua habilidade de sobrevida subseqüentes a ciclos de infecção com P. berghei e cura pelo Fansidar.


Mycobacterium bovis (BCG) significantly enhanced the development of immunity by CFW, C57BL/6, C57BL/10ScN and BALB/c (Nu+) mice to the erythrocytic stages of P. berghei. Mice treated with BCG required fewer cycles of infection and Pansidar (pyrimethamine + sulfadoxine) cure in order to develop solid immunity than untreated, immunized mice. However, those, mice treated with BCG at 30 days before the initiation of immunization showed an earliear loss of immunity to P. berghei than those mice which received BCG at 14 days or no BCG. Thus, BCG enhanced the host immune response to P. berghei during an initial infection, but shortened the length of immunity so that mice were more susceptible to P. berghei during subsequent infections. Treatment of CFW, BALR/c and C57BL/6 mice with bacterial lipopolysaccharide or hydrocortisone acetate (HDC) caused the animals to require more cycles of infections and drug cure in order to attain immunity than controls. Treatment of immunized C57BTV lOScN mice with hydrocortisone completely abolished their ability to survive a P. berghei infection.

Mycobacterium bovis; BCG; Bacterial Lipopolysaccharide Immunity to Plasmodium berghei; Effect of Hydrocortisone Mlycobacteriosis


ARTIGOS ORIGINAIS

Effects of mycobacterium bovis BCG, bacterial lipopolysaccharide and hydrocortisone on the development of immunity to Plasmodium berghei(* (* ) This study is based on a dissertation submitted By J. J. Ferraroni to Graduate School of the University of Montana in partial fulfillment of the requirements for the Doctor of Philosophy degree. )

Efeito do Mycobacterium bovis BCG, lipopolissacarideo bacteriano e hidrocortisona no desenvolvimento de imunidade ao Plasmodium berghei em camundongos

José J. FerraroniI, II; Thomas G. DouglassII; Clarence A. SpeerII

IUniversidade do Amazonas/CNFq, Campus Universitário, Departamento de Patologia - ICB - 69.000, Manaus, Amazonas, Brasil

IIDepartment of Microbiology, University of Montana, Missoula, Montana 59812, USA

SUMMARY

Mycobacterium bovis (BCG) significantly enhanced the development of immunity by CFW, C57BL/6, C57BL/10ScN and BALB/c (Nu+) mice to the erythrocytic stages of P. berghei. Mice treated with BCG required fewer cycles of infection and Pansidar (pyrimethamine + sulfadoxine) cure in order to develop solid immunity than untreated, immunized mice. However, those, mice treated with BCG at 30 days before the initiation of immunization showed an earliear loss of immunity to P. berghei than those mice which received BCG at 14 days or no BCG. Thus, BCG enhanced the host immune response to P. berghei during an initial infection, but shortened the length of immunity so that mice were more susceptible to P. berghei during subsequent infections. Treatment of CFW, BALR/c and C57BL/6 mice with bacterial lipopolysaccharide or hydrocortisone acetate (HDC) caused the animals to require more cycles of infections and drug cure in order to attain immunity than controls. Treatment of immunized C57BTV lOScN mice with hydrocortisone completely abolished their ability to survive a P. berghei infection.

Key words: Mycobacterium bovis — BCG — Bacterial Lipopolysaccharide Immunity to Plasmodium berghei — Effect of Hydrocortisone Mlycobacteriosis.

RESUMO

Mycobacterium bovis (BCG) aumenta significantemente o desenvolvimento da imunidade nos camundongos CFW, C57BL/6, C57BL/l0ScN e BALB/c (Nu/+) para os estágios eritrocitos do Plasmodium berghei. Camundongos tratados com BCG requerem menos ciclos de infecção com P. berghei e cura pelo Fansidar (pirimetamina + sulfadoxina) para desenvolverem imunidade sólida a este parasita do que os controles. Contudo, os animais que receberam BCG 30 dias antes do início da imunização evidenciaram uma perda precoce da imunidade adquirida para o P. berghei, quando comparado com os animais que receberam BCG 14 dias antes ou que não receberam BCG. Assim, sendo, o BCG aumentada a indução na resposta imune do hospedeiro ao P. berghei no curso de infecções subseqüentes. O tratamento de camundongos CFW, BALB/c e C57BL/6 com lipopolissacarídeo bacteriano ou hidrocortisona faz com que os animais requeiram um número maior de ciclos de infecção e cura para tornarem-se imunes ao P. berghei que os controles. O tratamento dos camundongos C57BL/10ScN com hidrocortisona aboliu completamente a sua habilidade de sobrevida subseqüentes a ciclos de infecção com P. berghei e cura pelo Fansidar.

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Recebido para publicação em 16-11-1983.

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  • Datas de Publicação

    • Publicação nesta coleção
      16 Out 2012
    • Data do Fascículo
      Fev 1986

    Histórico

    • Recebido
      16 Nov 1983
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