Navegando por Assunto "Malária cerebral"

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Acesso aberto (Open Access)
Alterações neuroquímicas no tecido retiniano murino em modelo de malária cerebral induzida pela infecção por Plasmodium berghei (ANKA)
(Universidade Federal do Pará, 2011-07-21) OLIVEIRA, Karen Renata Matos; NASCIMENTO, José Luiz Martins do; http://lattes.cnpq.br/7216249286784978
Cerebral Malaria (CM) is a severe complication resulting from Plasmodium falciparum infection. This condition has usually been associated with cognitive, behavioral and motor dysfunctions, being the retinopathy the most serious consequence resulting from the disease. The pathophysiologymechanisms underlying the complications of CM remain incompletely understood. Several experimental models of CM have already been developed in order to clarify those mechanisms related to this syndrome. In this context, the present work has been performed to investigate which possible neurochemistry alteration could be involved in the CM pathology. Male and female susceptible C57Bl/6 mice (6-8 week old) infected with ≈106 parasitized red blood cells (PbA), showed a low parasitaemia (15-20%), with evident clinical signs as: respiratory failure, ataxia, hemiplegia, and coma followed by animal death. In parallel to the clinical characterization of CM, retinal analysis demonstrated that the disease led to a decrease in the glutathione levels with 2 days post inoculation. However, this decrease was not so evident with the course of the infection (4º and 6º days post- infection). We further demonstrated that the increase in the glutathione levels during the infection is followed by the increase in the 3H-glutamate uptake rate (4º and 6º days post-infection), suggesting that CM condition causes an up-regulation of the transporters systems. Immunofluorescence data demonstrated that besides the activity increases, CM condition also stimulated the increase of the xCG- system expression in the retinal tissue. Furthermore, our findings also highlighted that in the retina the neurochemistries alterations occurs in a manner independent on the establishment of an inflammatory response, once TNF-α levels and NOS-2 expression were altered only in the cerebral tissue.
Acesso aberto (Open Access)
Avaliação dos níveis extracelulares de GABA e glutamato no sistema nervoso central de camundongos infectados com Plasmodium berghuei ANKA
(Universidade Federal do Pará, 2024-11) LIMA, Renato Mateus Santos de; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
Cerebral malaria (CM) caused by Plasmodium falciparum results in high mortality, especially in children under 5, with up to 25% of survivors experiencing neurological sequelae such as cognitive impairment and seizures. The neurochemical mechanisms behind these impairments are not well understood. This study aimed to characterize changes in the levels of the neurotransmitters glutamate (GLU) and γ-Aminobutyric acid (GABA) in the central nervous system (CNS) during experimental cerebral malaria (ECM). ECM was induced in Swiss mice with Plasmodium berghei ANKA (PbA), and the animals were monitored for parasitemia, survival, and neurological impairments using the Rapid Murine Coma and Behavior Scale (RMCBS). On the 7th day post-infection (d.p.i), blood-brain barrier (BBB) disruption was assessed using Evans Blue dye, and glial cell evaluation was performed by immunofluorescence. Results showed that PbA-infected mice began to succumb to CM by the 6th d.p.i, with 100% mortality by the 10th d.p.i. Behavioral impairments were observed from the early stages of infection. Significant BBB permeability changes and increased expression of glial activation markers were noted in infected mice. There was a marked increase in GLU levels in the brain and cerebellum on days 3, 5, and 7 post-infection. GABA levels increased on days 3 and 5, returning to control levels by day 7. These findings indicate significant neurochemical alterations in GABAergic and glutamatergic neurotransmission, accompanied by neurological and vascular impairments, suggesting their involvement in the development of neurological symptoms in CM.
Acesso aberto (Open Access)
Caracterização da resposta inflamatória e alterações neuroquímicas e eletrofisiológicas do tecido retiniano em modelo murino de malária cerebral induzido pela infecção por Plasmodium Berghei ANKA
(Universidade Federal do Pará, 2015-02-19) LEÃO, Luana Ketlen Reis; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
Cerebral malaria (CM) is one of the most serious complications resulting from infection by P. falciparum and the leading cause of death in children. The CM frame has a complex pathogenesis associated with neurological complications arising in an enhanced immune response as well as hemorrhagic events. Studies describing retinopathy associated with the frame, together with an intense process of astrogliosis in the vicinity of retinal vessels that nourish the tissue. This paper sought to characterize the inflammatory process and the possible neurochemical and electrophysiological changes in the retinal tissue of Swiss albino mice, when inoculated with Plasmodium berghei ANKA strain (PbA). Swiss albino mice were infected with PbA strain. To characterize the above experimental cerebral malaria (ECM) was evaluated several parameters, such as onset of clinical signs, survival curves parasitemia (%) and body mass gain, vascular permeability and quantification of cytokines (TNF-α, IL-6 and IL-10) in the cortical tissue. To evaluate changes in retinal tissue functionality, use full-field electroretinography. For the evaluation of neurotransmitter systems release assay was performed and uptake of glutamate and GABA which was then quantified by High Performance Liquid Chromatography. The inflammatory response analysis was performed to quantify the cytokines (TNF-α, IL-6 and IL-10) in retinal tissue. After characterizing the MCE framework we observe a reduction in the amplitude of b-wave of rods and cones, as well as increase the implicit time of rods, mixed responses at different intensities and oscillatory potential. We observed an increase in the release and glutamate uptake and also the activation of an anti-inflammatory pathway in retinal tissue. This study allowed us to validate the murine model of MCE and characterize for the first time, changes in the retinal function accompanied by changes in the glutamatergic system as well as activation of the inflammatory pathway in retinal tissue.