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Microglial cell‐derived interleukin‐6 influences behavior and inflammatory response in the brain following traumatic brain injury
Author(s) -
Sanchis Paula,
FernándezGayol Olaya,
Vizueta Joel,
Comes Gemma,
Canal Carla,
Escrig Anna,
Molinero Amalia,
Giralt Mercedes,
Hidalgo Juan
Publication year - 2020
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.23758
Subject(s) - microglia , traumatic brain injury , central nervous system , neuroscience , biology , lesion , interleukin , cytokine , cx3cr1 , inflammation , interleukin 6 , immunology , neuroinflammation , medicine , chemokine , pathology , chemokine receptor , psychiatry
Traumatic brain injury (TBI) is a major health problem with high rates of mortality and morbidity worldwide. The response of the brain to TBI is orchestrated by a number of cytokines, including interleukin‐6 (IL‐6). IL‐6 is a major cytokine in the central nervous system and it is produced by different cells, such as neurons, glial cells, and endothelial cells. Since glial cells are one of the most important sources and targets of IL‐6, we have examined the role of microglia‐derived IL‐6 in normal conditions and following a model of TBI, cryolesion of the somatosensorial cortex. To this end, tamoxifen‐inducible microglial IL‐6‐deficient ( Il6 ΔMic , using Cx3cr1 CreER model) mice and control ( Il6 lox/lox ) mice were used. In normal conditions, microglial IL‐6 deficiency reduced deambulation and exploratory behavior and decreased anxiety in a sex‐dependent manner. The transcriptome profile following cryolesion was dramatically altered 1 day post‐lesion in Il6 ΔMic compared with Il6 lox/lox mice. However, the phenotype of Il6 ΔMic mice was less compromised in the following days, suggesting that compensatory mechanisms are at play.