Poststroke Neuropsychiatric Symptoms : Relationships with IL-17 and Oxidative Stress

Stroke variably activates interleukin- (IL-) 17 expression, reduces regulatory T cells, and induces oxidative stress, which may support neurodegeneration. Ischemic stroke patients were screened for depressive symptoms (Center for Epidemiological Studies Depression (CES-D)) and cognitive status (Mini...

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Veröffentlicht in:BioMed research international 2014-01, Vol.2014 (2014), p.1-6
Hauptverfasser: Herrmann, Nathan, Swartz, R. H., Swardfager, W., Lanctôt, Krista L., Black, S. E., Khan, M. M., Andreazza, A. C.
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Sprache:eng
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Zusammenfassung:Stroke variably activates interleukin- (IL-) 17 expression, reduces regulatory T cells, and induces oxidative stress, which may support neurodegeneration. Ischemic stroke patients were screened for depressive symptoms (Center for Epidemiological Studies Depression (CES-D)) and cognitive status (Mini Mental State Examination). Proinflammatory cytokines (IL-17, IL-23, and interferon- [IFN-] γ), anti-inflammatory cytokine IL-10, and lipid hydroperoxide (LPH), a measure of oxidative stress, were assayed from fasting serum. Of 47 subjects (age 71.8 ± 14.4 years, 36% female), 19 had depressive symptoms (CES-D ≥ 16), which was associated with poorer cognitive status (F1,46=8.44, P=0.006). IL-17 concentrations did not differ between subjects with and without depressive symptoms (F1,46=8.44, P=0.572); however, IL-17 was associated with poorer cognitive status in subjects with depressive symptoms (F1,46=9.29, P=0.004). In those subjects with depressive symptoms, IL-17 was associated with higher LPH (ρ=0.518, P=0.023) and lower IL-10 (ρ=-0.484, P=0.036), but not in those without. In conclusion, poststroke depressive symptoms may be associated with cognitive vulnerability to IL-17 related pathways, involving an imbalance between proinflammatory and anti-inflammatory activity and increased oxidative stress.
ISSN:2314-6133
2314-6141
DOI:10.1155/2014/245210