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

• Autor(a) principal: Ferraroni, José J.
• Data de Publicação: 1986
• Outros Autores: Douglass, Thomas G., Speer, Clarence A.
• Tipo de documento: Artigo
• Idioma: por
• Título da fonte: Revista do Instituto de Medicina Tropical de São Paulo
• Texto Completo: https://www.revistas.usp.br/rimtsp/article/view/87460

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.