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.

Texto completo disponível apenas em PDF.

Full text available only in PDF format.

Recebido para publicação em 16-11-1983.

  • 1. BAZAR-MALIK, G. increased resistance to malaria ther Mycobacteria tuberculosis infection. Indian J. Med. Res. 61: 1014-1024, 1973.
  • 2. BLANDEN. R. V.; LEFFORD, M. J. & MACKANESS, G. B. The host response to Calmette-Guérin bacillus infection in mice. J. Exp. Med. 139: 1073-1101, 1969.
  • 3. BRAUDE, A. I. Absorption, distribution and elimination of endotoxins and their derivatives. In: Bacterial Endotoxins M. Candy and W. Braun (eds). New Jersey. Institute of Microbiology, Rutgers, the State University, 1964, 98-109.
  • 4. BROW, K. N.; BROWN, I. N. & HILLS, L. A. -Immunity to malaria. I Protection against Plasmodium knowlesi shown by monkeys sensitized with drugsuppressed infections or by dead parasites in Freund's adjuvant. Exp. Parasitol. 28: 304-317, 1970.
  • 5. BUTCHER, G. A.; MITCHELL, G. H. & COHEN, S. Antibody mediated mechanisms of immunity to malaria induced by vaccination with Plasmodium knowlesi merozoites. Immunology 34: 77-86, 1978.
  • 6. CLAMAN, H. N. Corticosteroid and lymphoid cells. New Engl. J. Med. 287: 388-397, 1972.
  • 7. CLARK, I. A.; ALLISON, A. C. &. Cox, F. E. C. Protection of mice against Babesia and Plasmodium with BCG. Nature 259: 309-311, 1976.
  • 8. CLARK. I. A.; COX, F. E. C. & ALLISON, A. C. Protection of mice, against Babesia spp and Plasmodium with killed Corynebacterium parvum Parasitology 74: 9-18, 19-77.
  • 9. COTRELL, B. J.; PLAYFAIR, J. H. L. & SOUZA, J. B. de - Plasmodium yoelil and Plasmodium vinckei: the effects of nonspecific .immunostimulation on murine malaria. Exp. Parasitol. 43: 45-53, 1977.
  • 10. ELING, W. Survival of parasites in mice immunized against Plasmodium berghei. Z. Tropemned. Parasitol. 29: 204-209, 1978.
  • 11. ELING, W. Plasmodium berghei: Premunition, sterile immunity, and loss of immunity in mice. Exp. Parasitol, 49: 89-96, 1980.
  • 12. FERRARONI, J. J. & SPEER, C. A. Fansidar prophylaxis, therapy and immune responses in rodent malaria (Plasmodium berghei) J. Parasitol. 68: 609-615, 1983.
  • 13. FINDLAY, G. M. & HOWARD, E. M. Cortisone and Plasmodium berghei infection in mice. Nature 169: 547, 1952.
  • 14. FINGER, H.; EMMERLING, P. & BUSSE, M. Increased priming for the secondary response in mice to sheep erythrocytes by bacterial endotoxins. Int. Arch. Allergy 38: 598-606. 1970.
  • 15. FREUND. J.; THONSON, K. J.; SOMMER, H. E.: WALTER. A. W. & SCHENKEIN. E. L. Immunization of Rhesus monkeys against malaria infection (Plasmodium knowlesi) with killed parasites and adjuvants. Science 103: 202-204. 1945.
  • 16. JONES, J. M. & KIND, P. D. Enhancing effects of bacterial endotoxins on bone marrow cells in the immune response to SRBC. J. Immunol. 108: 1453-1455, 1972.
  • 17. LAGRANGE. P. H-; MACKANESS, G. B.; MILLER, T. E. A PARDON, P. Effects of the induction and expression of cell-mediated immunity. I Depression of the afferent arm. J. Immunol. 114: 442-446, 1975.
  • 18. MACGREGOR, R. R.: SHEAGREN, J. N. & WOLFF. S. M. Endotoxin-induced modification of Plasmodium berghei infection in mice. J. Immunol. 102: 131-139, 1969.
  • 19. MACKANESS, G. B.; LAGRANGE. P. H.; MILLER, T. E. & ISHIBASHI, T. Feedback inhibition of specifically sensitized lymphocytes. J. Exp. Med. 139: 543-549, 1974.
  • 20. MARTIN, L. K.; EINHEBER. A.; SADUN. E. H. & WREN, R. E. Effect of bacterial endotoxin on the course of Plasmodium berghei infection. Exp. Parasitol. 20: 186-199, 1967.
  • 21. MITCHELL, G. H. A review of merozoite vaccination against Plasmodium knowlesi malaria. Trans. R. Soc. Trop. Med. Hyg. 71: 281-282, 1977.
  • 22. MURPHY, J. Host defenses in murine malaria: No specific resistance to Plasmodium berghei generated in response to Mycobacterium bovis infection or Corynebacterium parvum stimulation. Infect. Immun. 33: 199-211, 1981.
  • 23. MURPHY, J. & LEPPORD, M. J. Host defenses in murine malaria. Successful vaccination of mice against Plasmodium berghei by using formalized blood parasites. Am. J. Trop. Med. Hyg. 28: 4-11, 1972.
  • 24. NUSSENZWEIG, R. S. Increased nonspecific resistance to malaria produced by administration of killed Corynebacterium parvum Exp. Parasitol. 21: 224-231, 1967.
  • 25. NUSSENZWEIG. R. S.; VANDERBERG, J. P. & MOST, H. Protective immunity produced by the injection of X-irradiated sporozoites of Plasmodium berghei IV. Dose response, specificity and humoral immunity. Milit. Med. 134: 1176-1182, 1969.
  • 26. REISEN, W. K. & HILLS, T. C. Failure to protect Mus musculus against Plasmodium berghei with footpad injection or killed parasites incorporated Id Freund's adjuvant. J. Parasitol. 61: 937-940. 1975.
  • 27. SCHENKEL, R. H.; CABRERA. E. J.; BARE, M. L. & SILVERMAN, P. H. A new adjuvant for use in vaccination against malaria. J. Parasitol. 61: 549-550, 1975.
  • 26. SINGER, I. The effect of cortisone on infections with Plasmodium berghei in the white mouse. J. Infect. Dis. 94: 164-172, 1954.
  • 29. SMRKOVSKI, L. Effect of route of Mycobacterium bovis (BCG) administration on induction of suppression of sporozoito immunity in rodent malaria. Infect. Immun. 31: 408-412, 1981.
  • 30. SMRKOVSKI, L. & STRICKLAND, G. Rodent malaria: BCG-induced protection and immunosuppression. J. Immunol. 121: 1257-1261, 1978.
  • 31. TAVERNE, J.; DOCKRELL, H. M. & PLAYFAIR, J. H. L. Endotoxin-induced serum factor kils malarial parasites in vitro. Infect. Immun. 33: 83-89, 1981.
  • 32. TOBIE, J. P.; WOLPP, S. M. & JEFFERY, G. M. Immune response of man to inoculation with Plasmodium cynomolgi and challenged with Plasmodium vivax Lancet 2: 300-303, 1966.
  • 33. WAKI, S. & SUZUKI, M. T-independent antibody production in nude mice immunized with a rodent malaria parasite (Plasmodium berghei). In N. D. Reed (ed). Proceedings of the 3rd International Workshop on Nude Mice. New York, Gustav Fisher. 1981.

  • (*
    ) 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.

Datas de Publicação

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

Histórico

  • Recebido
    16 Nov 1983
Instituto de Medicina Tropical de São Paulo Av. Dr. Enéas de Carvalho Aguiar, 470, 05403-000 - São Paulo - SP - Brazil, Tel. +55 11 3061-7005 - São Paulo - SP - Brazil
E-mail: revimtsp@usp.br