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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/20772

Title: Maternal immune activation evoked by polyinosinic:polycytidylic acid does not evoke microglial cell activation in the embryo.
Authors: Smolders, Silke
Smolders, Sophie M.T.
Swinnen, Nina
Gärtner, Annette
Rigo, Jean-Michel
Legendre, Pascal
Brône, Bert
Issue Date: 2015
Citation: Frontiers in cellular neuroscience, 9
Abstract: Several studies have indicated that inflammation during pregnancy increases the risk for the development of neuropsychiatric disorders in the offspring. Morphological brain abnormalities combined with deviations in the inflammatory status of the brain can be observed in patients of both autism and schizophrenia. It was shown that acute infection can induce changes in maternal cytokine levels which in turn are suggested to affect fetal brain development and increase the risk on the development of neuropsychiatric disorders in the offspring. Animal models of maternal immune activation reproduce the etiology of neurodevelopmental disorders such as schizophrenia and autism. In this study the poly (I:C) model was used to mimic viral immune activation in pregnant mice in order to assess the activation status of fetal microglia in these developmental disorders. Because microglia are the resident immune cells of the brain they were expected to be activated due to the inflammatory stimulus. Microglial cell density and activation level in the fetal cortex and hippocampus were determined. Despite the presence of a systemic inflammation in the pregnant mice, there was no significant difference in fetal microglial cell density or immunohistochemically determined activation level between the control and inflammation group. These data indicate that activation of the fetal microglial cells is not likely to be responsible for the inflammation induced deficits in the offspring in this model.
Notes: BIOMED - Hasselt University Hasselt, Belgium ; Laboratory of Neuronal Differentiation, VIB Center for the Biology of Disease, Leuven and Center for Human Genetics, KU Leuven Leuven, Belgium.
URI: http://hdl.handle.net/1942/20772
DOI: 10.3389/fncel.2015.00301
ISSN: 1662-5102
Category: A1
Type: Journal Contribution
Validation: vabb, 2017
Appears in Collections: Research publications

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