Experimental sepsis-associated encephalopathy is accompanied by altered cerebral blood perfusion and water diffusion and related to changes in cyclooxygenase-2 expression and glial cell morphology but not to blood-brain barrier breakdown
| Autor: | Renaud Nicolas, Bassem Hiba, Olivier Periot, Marion Griton, Jan Pieter Konsman, Ibtihel Dhaya, Gérard Raffard |
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| Přispěvatelé: | Institut des sciences cognitives Marc Jeannerod - Centre de neuroscience cognitive - UMR5229 (CNC), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Institut de Neurosciences cognitives et intégratives d'Aquitaine (INCIA), Université Bordeaux Segalen - Bordeaux 2-Université Sciences et Technologies - Bordeaux 1-SFR Bordeaux Neurosciences-Centre National de la Recherche Scientifique (CNRS), Centre de résonance magnétique des systèmes biologiques (CRMSB), Centre National de la Recherche Scientifique (CNRS)-Université de Bordeaux (UB) |
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Pathology medicine.medical_specialty [SDV]Life Sciences [q-bio] Immunology Encephalopathy Corpus callosum Blood–brain barrier Cell morphology Diffusion White matter 03 medical and health sciences Behavioral Neuroscience [SPI]Engineering Sciences [physics] 0302 clinical medicine medicine Animals Rats Wistar ComputingMilieux_MISCELLANEOUS Aquaporin 4 Endocrine and Autonomic Systems Chemistry Water Sepsis-Associated Encephalopathy medicine.disease Rats Perfusion 030104 developmental biology medicine.anatomical_structure nervous system Cerebral blood flow Blood-Brain Barrier Cyclooxygenase 2 Immunoglobulin G Cell activation Neuroglia 030217 neurology & neurosurgery |
| Zdroj: | Brain, Behavior, and Immunity Brain, Behavior, and Immunity, Elsevier, 2020, 83, pp.200-213. ⟨10.1016/j.bbi.2019.10.012⟩ |
| ISSN: | 0889-1591 1090-2139 |
| DOI: | 10.1016/j.bbi.2019.10.012⟩ |
| Popis: | Sepsis-associated encephalopathy (SAE) refers to brain dysfunction, including delirium, occurs during severe infection and is associated with development of post-traumatic stress disorder. SAE has been proposed to be related to reduced cerebral blood flow (CBF), blood-brain barrier breakdown (BBB), white matter edema and disruption and glia cell activation, but their exact relationships remain to be determined. In the present work, we set out to study CBF using Arterial Spin Labeling (ASL) and grey and white matter structure with T2- and diffusion magnetic resonance imaging (dMRI) in rats with cecal ligation and puncture (CLP)-induced encephalopathy. Using immunohistochemistry, the distribution of the vasoactive prostaglandin-synthesizing enzyme cyclooxygenase-2 (COX-2), perivascular immunoglobulins G (IgG), aquaporin-4 (AQP4) and the morphology of glial cell were subsequently assessed in brains of the same animals. CLP induced deficits in the righting reflex and resulted in higher T2-weighted contrast intensities in the cortex, striatum and at the base of the brain, decreased blood perfusion distribution to the cortex and increased water diffusion parallel to the fibers of the corpus callosum compared to sham surgery. In addition, CLP reduced staining for microglia- and astrocytic-specific proteins in the corpus callosum, decreased neuronal COX-2 and AQP4 expression in the cortex while inducing perivascular COX-2 expression, but did not induce widespread perivascular IgG diffusion. In conclusion, our findings indicate that experimental SAE can occur in the absence of BBB breakdown and is accompanied by increased water diffusion anisotropy and altered glia cell morphology in brain white matter. |
| Databáze: | OpenAIRE |
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