RESUMO
Immunosuppression has been reported to occur during active visceral leishmaniasis and some factors such as the cytokine profile may be involved in this process. In the mouse model of cutaneous leishmaniasis using Leishmania (Leishmania) major, the Th1 response is related to protection while the Th2 response is related to disease progression. However, in hamsters, which are considered to be an excellent model for the study of visceral leishmaniasis, this dichotomy is not observed. Using outbred 45- to 60-day-old (140 to 150 g) male hamsters infected intraperitoneally with 2 x 10(7) L. (L.) chagasi amastigotes, we evaluated the immune response of spleen cells and the production of cytokines. We used 3 to 7 hamsters per group evaluated. We detected a preserved response to concanavalin A measured by index of proliferation during all periods of infection studied, while a proliferative response to Leishmania antigen was detected only at 48 and 72 h post-infection. Messenger RNA from cytokines type 1 (IL-2, TNF-α, IFN-γ) and type 2 (IL-4, IL-10 and TGF-β) detected by reverse transcriptase polymerase chain reaction and produced by spleen cells showed no qualitative difference between control non-infected hamsters and infected hamsters during any period of infection evaluated. Cytokines were measured by the DNA band intensity on agarose gel using the Image Lab 1D L340 software with no differences observed. In conclusion, the present results showed an antigen-dependent immunosuppression in hamsters with active visceral leishmaniasis that was not related to the cytokine profile.
Assuntos
Animais , Cricetinae , Masculino , Camundongos , Antígenos de Protozoários/imunologia , Citocinas/imunologia , Tolerância Imunológica/imunologia , Leishmania/imunologia , Leishmaniose Visceral/imunologia , Linfócitos T/imunologia , Proliferação de Células/efeitos dos fármacos , Modelos Animais de Doenças , Fator de Crescimento Transformador beta , Fatores de Crescimento Transformadores/imunologiaRESUMO
A esclerose múltipla (EM) é uma doença do sistema nervoso central (SNC) na qual há destruiçäo da bainha de mielina e reaçäo inflamatória local. Acredita-se que seja uma resposta auto-imune desencadeada por fatores ambientais que induzem a superexpressäo de citocinas em indivíduos geneticamente predispostos. As citocinas implicadas nas exarcebações da EM, tais como IL-1, IL-2, IL-3, INFðy, TNF-alfa e TNF-ß, induzem a expressäo de moléculas específicas na membrana das células do SNC e ativam a funçäo fagocítica das células da micróglia