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Effects of Ethanol on Immune Response in the Brain: Region‐Specific Changes in Adolescent Versus Adult Mice
Author(s) -
Kane Cynthia J. M.,
Phelan Kevin D.,
Douglas James C.,
Wagoner Gail,
Johnson Jennifer W.,
Xu Jihong,
Phelan Patrick S.,
Drew Paul D.
Publication year - 2014
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.12244
Subject(s) - glial fibrillary acidic protein , astrocyte , hippocampus , endocrinology , neuroinflammation , medicine , synaptophysin , neuropathology , cerebellum , immunostaining , neurodegeneration , biology , neuroscience , central nervous system , immunohistochemistry , inflammation , disease
Background Alcohol use occurs across the life span beginning in adolescence and continuing through adulthood. Ethanol ( E t OH )‐induced pathology varies with age and includes changes in neurogenesis, neurodegeneration, and glial cell activation. E t OH ‐induced changes in glial activation and immune activity are believed to contribute to E t OH ‐induced neuropathology. Recent studies indicate an emerging role of glial‐derived neuroimmune molecules in alcohol abuse and addiction. Methods Adolescent and adult C 57 BL /6 mice were treated via gavage with 6 g/kg E t OH for 10 days, and tissue was harvested 1 day post treatment. We compared the effects of E t OH on chemokine and cytokine expression and astrocyte glial fibrillary acidic protein ( GFAP ) immunostaining and morphology in the hippocampus, cerebellum, and cerebral cortex. Results E t OH increased m RNA levels of the chemokine CCL 2/ MCP ‐1 in all 3 regions of adult mice relative to controls. The cytokine interleukin‐6 ( IL ‐6) was selectively increased only in the adult cerebellum. E t OH did not affect m RNA levels of the cytokine tumor necrosis factor‐alpha (TNF‐α) in any of these brain regions in adult animals. Interestingly, CCL 2, IL ‐6, and TNF ‐α m RNA levels were not increased in the hippocampus, cerebellum, or cortex of adolescent mice. E t OH treatment of adult and adolescent mice resulted in increased GFAP immunostaining. Conclusions Collectively, these data indicate an age‐ and region‐specific susceptibility to E t OH regulation of neuroinflammatory and addiction‐related molecules as well as astrocyte phenotype. These studies may have important implications concerning differential alcohol‐induced neuropathology and alcohol addiction across the life span.