Shujuan Li1, Qingqing Dai2, Jinling Yu2, Ting Liu2, Shuiqiao Liu2, Longhui Ma2, Ying Zhang2, Song Han2, Junfa Li2. 1. a Department of Neurology , Beijing Chao-Yang Hospital, Capital Medical University , Beijing , PR China. 2. b Department of Neurobiology and Center of Stroke , Beijing Institute for Brain Disorders, Capital Medical University , Beijing , PR China.
Abstract
BACKGROUND: Interleukin (IL)-17A was reported to be involved in the development of post-ischemic stroke inflammatory response and functional recovery. However, the IL-17A dynamic changes in serum/cerebrospinal fluid (CSF) and its role in neuronal injury following ischemic stroke are unclear. METHODS: In vivo ischemic stroke was induced by 1 h of middle cerebral artery occlusion (MCAO) and 6 h-7 d reperfusion (R) in mice, while in vitro stroke was induced by 1 h oxygen-glucose deprivation (OGD)/24 h reoxygenation (R) in cultured cortical neurons. Enzyme-linked immunosorbent assay (ELISA) and double-labeled immunofluorescence of IL-17A with neuron (NeuN), astrocyte (GFAP) and microglia (Iba-1)-specific markers were used to determine the IL-17A levels in serum/CSF and neural cell type. RESULTS: The ELISA results showed that IL-17A significantly increased both in peri-infarct region (p < 0.001) and CSF (p < 0.05) following 1 h MCAO/R 12 h. The levels of IL-17A in serum increased at R 1 d (p < 0.05) and peaked at R 3 d (p < 0.001) after 1 h MCAO. Immunofluorescent staining demonstrated that IL-17A co-localized with GFAP in peri-infarct regions. In addition, recombinant rIL-17A could aggravate ischemic injuries at dose-dependent manner in 1 h OGD/R 24 h-treated neurons companying with the increase of IL-17A receptor il-17RA mRNA (p < 0.001) and IL-17R protein levels. CONCLUSION: We firstly reported astrocytic IL-17A peaks in CSF within 12 h and in serum at 3 d reperfusion after ischemic stroke. IL-17A may exaggerate neuronal injuries through its receptor IL-17R at early stage of ischemic stroke.
BACKGROUND:Interleukin (IL)-17A was reported to be involved in the development of post-ischemic stroke inflammatory response and functional recovery. However, the IL-17A dynamic changes in serum/cerebrospinal fluid (CSF) and its role in neuronal injury following ischemic stroke are unclear. METHODS: In vivo ischemic stroke was induced by 1 h of middle cerebral artery occlusion (MCAO) and 6 h-7 d reperfusion (R) in mice, while in vitro stroke was induced by 1 h oxygen-glucose deprivation (OGD)/24 h reoxygenation (R) in cultured cortical neurons. Enzyme-linked immunosorbent assay (ELISA) and double-labeled immunofluorescence of IL-17A with neuron (NeuN), astrocyte (GFAP) and microglia (Iba-1)-specific markers were used to determine the IL-17A levels in serum/CSF and neural cell type. RESULTS: The ELISA results showed that IL-17A significantly increased both in peri-infarct region (p < 0.001) and CSF (p < 0.05) following 1 h MCAO/R 12 h. The levels of IL-17A in serum increased at R 1 d (p < 0.05) and peaked at R 3 d (p < 0.001) after 1 h MCAO. Immunofluorescent staining demonstrated that IL-17A co-localized with GFAP in peri-infarct regions. In addition, recombinant rIL-17A could aggravate ischemic injuries at dose-dependent manner in 1 h OGD/R 24 h-treated neurons companying with the increase of IL-17A receptor il-17RA mRNA (p < 0.001) and IL-17R protein levels. CONCLUSION: We firstly reported astrocytic IL-17A peaks in CSF within 12 h and in serum at 3 d reperfusion after ischemic stroke. IL-17A may exaggerate neuronal injuries through its receptor IL-17R at early stage of ischemic stroke.