Asunto(s)
Enfermedades de los Ganglios Basales/genética , Enfermedades de los Ganglios Basales/patología , Neurodegeneración Asociada a Pantotenato Quinasa/genética , Fosfotransferasas (Aceptor de Grupo Alcohol)/genética , Adolescente , Adulto , Edad de Inicio , Enfermedades de los Ganglios Basales/epidemiología , Química Encefálica , Brasil/epidemiología , Niño , Preescolar , Trastornos Distónicos/diagnóstico , Trastornos Distónicos/genética , Femenino , Trastornos Heredodegenerativos del Sistema Nervioso/epidemiología , Trastornos Heredodegenerativos del Sistema Nervioso/genética , Humanos , Hierro/metabolismo , Imagen por Resonancia Magnética , Masculino , Mutación , Adulto JovenRESUMEN
Earlier studies had shown that the viscerotropic NIH 173 strain of cutaneous Leishmania major fails to come under Lsh gene control. Visceral Leishmania donovani LV9 and another viscerotropic cutaneous strain, Leishmania mexicana mexicana LV4, are controlled by Lsh. The results of double-infection experiments presented here show that expression of Lsh resistance against L. mexicana mexicana was enhanced in the presence of L. donovani, whereas L. major still failed to come under Lsh gene control, even in the presence of L. donovani. Prior irradiation (850 rads) of mice showed that in the absence of infiltrating monocytes, Lsh did exert some influence over L. major. The presence of a higher infiltrate of fresh monocytes after L. major infection was confirmed in liver macrophage populations isolated from mice after infection in vivo and in liver cryosections immunostained with monoclonal antibody M1/70 directed against the type 3 complement receptor CR3. The results support the hypothesis that Lsh is expressed maximally in the resident tissue macrophages and poorly in the immature macrophages preferentially infected by L. major amastigotes.