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Microb Pathog ; 117: 299-303, 2018 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-29496525

RESUMO

Malaria is a harmful disease affecting both tropical and subtropical countries and causing sometimes fatal complications. The effects of malaria-related complications on the intestine have been relatively neglected, and the reasons for the intestinal damage caused by malaria infection are not yet clear. The present study aims to evaluate the influence of intestinal vitamin D receptor on host-pathogen interactions during malaria induced in mice by Plasmodium chabaudi. To induce the infection, animals were infected with 106P. chabaudi-parasitized erythrocytes. Mice were sacrificed on day 8 post-infection. The infected mice experienced a significant body weight loss and parasitaemia affecting about 46% of RBCs. Infection caused marked pathological changes in the intestinal tissue indicated by shortening of the intestine and villi. Moreover, the phagocytic activity of macrophages increased significantly (P < 0.01) in the infected villi compared to the non-infected ones. Infection by the parasite also induced marked upregulation of nuclear factor-kappa B, inducible nitric oxide synthase, Vitamin D Receptor, interleukin-1ß, tumour necrosis factor alpha and interferon gamma-mRNA. It can be implied from this that vitamin D receptor has a role in regulating malarial infection.


Assuntos
Interações Hospedeiro-Parasita/fisiologia , Mucosa Intestinal/metabolismo , Malária/sangue , Malária/complicações , Plasmodium chabaudi/patogenicidade , Receptores de Calcitriol/fisiologia , Animais , Peso Corporal , Modelos Animais de Doenças , Eritrócitos/parasitologia , Eritrócitos/patologia , Feminino , Regulação da Expressão Gênica , Interações Hospedeiro-Parasita/genética , Interferon gama/metabolismo , Interleucina-1beta/metabolismo , Intestinos/parasitologia , Intestinos/patologia , Macrófagos/metabolismo , Malária/parasitologia , Malária/patologia , Camundongos , Camundongos Endogâmicos C57BL , Subunidade p50 de NF-kappa B/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Parasitemia , Fagocitose , RNA Mensageiro/biossíntese , Fator de Necrose Tumoral alfa/metabolismo
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