Histological and histomorphometric evaluation of the retina of mice infected with Schistosoma mansoni in its hepatosplenic form / Avaliação histológica e histomorfométrica da retina de camundongos infectados pelo Schistosoma mansoni na forma hepatoesplênica

PURPOSE: To evaluate retinal manifestations of Schistosomiasis mansoni in its hepatosplenic form in mice. METHODS: It was performed a study with two groups of mice; one of them was infected with 40 cercariae of Schistosoma mansoni. After 120 days of the infection, the eyes underwent a retinal microscopy study. The histology findings were reported. Histomorphometric analysis was also performed, including: thickness measurement of the retinal layer and the number of the ganglion layer cells. RESULTS: In one case a retinal granuloma was found. The analysis of the other histological sections demonstrated normal architecture of the retina. The mean thickness of the retinal layer between the two groups were similar (41.81±6.09µm versus 38.48±8.58µm - p=0.279); as well as the mean number of the ganglion layer cells (20.93±4.88 versus 20.64±4.10 - p=0.864). Disorganization of the retinal layers was not identified and the histomorphometric analysis revealed no significant difference between the two groups. CONCLUSION: The absence of findings in this study does not exclude that hemodynamic and autoregulation changes associated with hepatosplenic schistosomiasis could be correlated to retinal manifestations. It is necessary that other methods with a high parasite infection should be performed.

OBJETIVO: Avaliar as repercussões da esquistossomose mansônica na forma hepatoesplênica na retina de camundongos. MÉTODOS: Foi realizado estudo com dois grupos de camundongos, sendo um infectado com 40 cercárias do Schistosoma mansoni. Decorridos 120 dias da infecção, os olhos foram submetidos à análise microscópica da retina com descrição dos achados histológicos e realizada análise histomorfométrica com mensuração da espessura de segmento retiniano e do número de células da camada ganglionar. RESULTADOS: Em um caso foi encontrado um granuloma retiniano. Já a análise dos demais cortes histológicos demonstrou uma arquitetura normal da retina. A média da espessura dos segmentos retinianos entre os grupos de camundongos, controle e infectado, foi similar (41,81±6,09µm versus 38,48±8,58µm - p=0,279) assim como a média do número de células da camada ganglionar (20,93±4,88 versus 20,64±4,10 - p=0,864). : A estrutura da retina encontrava-se íntegra e a análise histomorfométrica não revelava diferença significante entre os dois grupos. CONCLUSÃO: A ausência de alterações, neste estudo, não afasta a possibilidade de que desequilíbrios hemodinâmicos e no mecanismo de autoregulação, em portadores da forma hepatoesplênica da esquistossomose, possam acarretar dano retiniano. Demanda, entretanto, que outras metodologias com indução da infecção com uma maior carga parasitária sejam realizadas.

Compromiso neuronal en esclerosis multiple / Neuronal injury in multiple sclerosis

La esclerosis múltiple (EM) ha sido considerada clásicamente como una enfermedad desmielinzante. Si bien el compromiso neurodegenerativo fue previamente descripto, sólo recientemente ha sido enfatizado. Por estudiosos recientes se ha identificado la degeneración axonal como el mayor determinante de discapacidad neurológica irreversible en pacientes con EM. El daño axonal se inicia tempranamente y permanece silente durante años, la discapacidad neurológica se desarrolla cuando se alcanza cierto umbral de pérdida axonal y los mecanismos de compensación se agotan. Se han propuesto tres hipótesis para explicar el daño axonal: 1) El daño es causado por un proceso inflamatorio, 2) Existe una excesiva acumulación de Ca2+ intra-axonal, 3) Los axones desmienlinizados evolucionan a un proceso degenerativo producto de la falta de soporte trófico provisto por la mielina o células formadoras de mielina. Si bien la EM fue tradicionalmente considerada como una enfermedad de la sustancia blanca, el proceso de desmielinización tambiém ocurre en la corteza cerebral

The concept of multiple sclerosis (MS) as a demyelinating disease is deeply ingrained. Although the existence of a neurodegenerative component has always been apparent, it has only recently become emphasized. Thus, in recent years several studies have identified axonal degeneration as the major determinant of irreversible neurological disability in patients with MS. Axonal injury begins at disease onset and remains clinically silent for many years; irreversible neurological disability develops when a threshold of axonal loss is reached and CNS compensatory mechanisms are exhausted. The precise mechanisms of axonal loss are poorly understood, and three hypotheses have been proposed: 1) The damage is caused by an inflammatory process, 2) There is an excessive accumulation of intra-axonal Ca2+, 3) Demyelinated axons undergo degeneration due to lack of trophic support by myelin, or myelin forming cells. Although MS has traditionally been regarded as a disease of white matter, demyelination can also occur in the cerebral cortex. Cortical lesions exhibit neuronal injury represented by dendritic and axonal transection as well as neuronal apoptosis. Because conventional nuclear magnetic resonance (NMR) is limited in its ability to provide specific information about axonal pathology in MS, new techniques such as, diffusion-weighted MRI, proton magnetic resonance spectroscopy, functional MRI, as well as novel techniques designed to measure atrophy have been developed to monitor MS evolution. Recognition that MS is in part a neurodegenerative disease should trigger critical rethinking on the pathogenic mechanisms of this disease and provides new targets for a rational treatment