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1.
Arq. neuropsiquiatr ; 75(2): 96-102, Feb. 2017. tab, graf
Article Dans Anglais | LILACS | ID: biblio-838865

Résumé

ABSTRACT Neurocysticercosis (NCC) is the most severe clinical manifestation of cysticercosis. One of the factors responsible for its symptomatology is the host inflammatory response. Therefore the influence of interleukin 4 (IL-4) on the induction of encephalitis in experimental NCC was evaluated. Methods BALB/c (WT) and BALB/c (IL-4-KO) mice were inoculated intracranially with Taenia crassiceps cysticerci and euthanized at 7, 30, 60 and 90 days later, the encephala removed and histopathologically analyzed. Results The absence of IL-4 induced greater parasitism. In the initial phase of the infection, IL-4-KO showed a lower intensity in the inflammatory infiltration of polimorphonuclear cells in the host-parasite interface and intra-parenquimatous edema. The IL-4-KO animals, in the late phase of the infection, showed lower intensity of ventriculomegaly, encephalitis, and meningitis, and greater survival of the parasites in comparison with the WT animals. Conclusion The absence of IL-4 induced lower inflammatory infiltration, ventriculomegaly and perivasculitis in experimental NCC.


RESUMO A Neurocisticercose (NCC) é a manifestação clínica mais severa da cisticercose, e um dos fatores responsáveis pela sintomatologia é a resposta inflamatória do hospedeiro. Desta forma avaliou-se a influência da interleucina 4 (IL-4) na indução de encefalite na NCC experimental. Métodos Camundongos das linhagens BALB/c (WT) e BALB/c (IL-4-KO) foram inoculados intracranialmente com cisticercos de Taenia crassiceps e eutanasiados aos 7, 30, 60 e 90 dias após a infecção, os encéfalos foram removidos e analisados histopatologicamente. Resultados A ausência da IL-4 induziu um maior parasitismo nos animais. Na fase inicial da infecção os animais IL-4-KO apresentaram menor intensidade tanto de infiltrado inflamatório de polimorfonucleares na interface parasito-hospedeiro quanto de edema intraparenquimatoso. Os animais IL-4-KO, na fase tardia, apresentaram menor intensidade de ventriculomegalia, encefalite, meningite e maior sobrevivência dos cisticercos em relação aos animais WT. Conclusão A ausência da IL-4 induz menos infiltrado inflamatório, ventriculomegalia e perivasculite na NCC experimental.


Sujets)
Animaux , Femelle , Rats , Encéphale/parasitologie , Interleukine-4/sang , Neurocysticercose/parasitologie , Cysticercus/physiologie , Encéphalite infectieuse/parasitologie , Facteurs temps , Neurocysticercose/sang , Modèles animaux de maladie humaine , Encéphalite infectieuse/sang , Interactions hôte-parasite , Souris de lignée BALB C
2.
Braz. j. infect. dis ; 20(2): 115-118, Mar.-Apr. 2016. tab
Article Dans Anglais | LILACS | ID: lil-780808

Résumé

Abstract Background/aims The frequency of Human Leucocyte Antigens/alleles associated with rapid progression from Human Immunodeficiency Virus infection to Acquired Immunodeficiency Syndrome was evaluated in Brazilian patients with Acquired Immunodeficiency Syndrome with and without Toxoplasmic Encephalitis. Methods 114 patients with Acquired Immunodeficiency Syndrome (41 with Toxoplasmic Encephalitis, 43 with anti-Toxoplasma gondii antibodies, without Toxoplasmic Eencephalitis, and 30 without anti-Toxoplasma gondii antibodies circulating and without Toxoplasmic Encephalitis) were studied. Results Human Leucocyte Antigens/alleles associated with rapid progression to Acquired Immunodeficiency Syndrome, particularly HLA-B35, -DR3, and -DR1 allele group, were significantly less represented in patients with Toxoplasmic Encephalitis and Acquired Immunodeficiency Syndrome. Conclusion The presence of these Human Leucocyte Antigens/Alleles that predispose to Acquired Immunodeficiency Syndrome progression was associated with resistance to Toxoplasmic Encephalitis among Human Immunodeficiency Virus-1 carriers.


Sujets)
Humains , Mâle , Femelle , Adulte , Adulte d'âge moyen , Jeune adulte , Syndrome d'immunodéficience acquise/sang , Toxoplasmose cérébrale/sang , Allèles , Encéphalite infectieuse/sang , Antigènes HLA/sang , Marqueurs biologiques/sang , Syndrome d'immunodéficience acquise/complications , Syndrome d'immunodéficience acquise/génétique , Toxoplasmose cérébrale/complications , Toxoplasmose cérébrale/génétique , Évolution de la maladie , Encéphalite infectieuse/génétique , Encéphalite infectieuse/parasitologie
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