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Title of Journal: Mol Neurobiol

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Abbravation: Molecular Neurobiology

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Springer US

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DOI

10.1007/978-1-4614-7479-1_40

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ISSN

1559-1182

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Il1β Involvement in Cognitive Impairment after Se

Authors: Francielle Mina Clarissa M Comim Diogo Dominguini Omar J CassolJr Dhébora M Dall`Igna Gabriela K Ferreira Milena C Silva Leticia S Galant Emílio L Streck João Quevedo Felipe DalPizzol
Publish Date: 2013/11/15
Volume: 49, Issue: 2, Pages: 1069-1076
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Abstract

Sepsis is defined as the hosts reaction to infection and characterised by a systemic inflammatory response with important clinical implications Central nervous system dysfunction secondary to sepsis is associated with local generation of pro and antiinflammatory cytokines impaired cerebral microcirculation an imbalance of neurotransmitters apoptosis and cognitive impairment Its known that the IL1β is one of the first cytokines to be altered Thus the objective of this study was to evaluate the role of IL1β in cognitive parameters in brain tissue through the use of an IL1β IL1ra receptor antagonist up to 10 days and to assess blood–brain barrier permeability cytokine levels oxidative parameters and energetic metabolism up to 24 h after sepsis induction To this aim we used shamoperated Wistar rats or submitted to the cecal ligation and perforation CLP procedure Immediately after the animals received one dose of 10 μg of IL1ra After 24 h the rats were killed and were evaluated for biochemical parameters in the prefrontal cortex hippocampus and striatum After 10 days the animals were submitted to the habituation to the open field and stepdown inhibitory avoidance task We observed that the use of IL1ra reverted the increase of blood–brain barrier permeability in the prefrontal cortex hippocampus and striatum the increase of IL1β IL16 and TNFα levels in the prefrontal cortex and striatum the decrease of complex I activity in the prefrontal hippocampus and striatum the increase of oxidative parameters in prefrontal cortex hippocampus and striatum and cognitive impairment In conclusion the results observed in this study reinforce the role of acute brain inflammatory response in particular the IL1β response in the cognitive impairment associated with sepsis

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