1. Interleukin-6, MCP-1, IP-10, and MIG are sequentially expressed in cerebrospinal fluid after subarachnoid hemorrhage.
- Author
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Aichi Niwa, Koji Osuka, Takahiro Nakura, Naoki Matsuo, Takeya Watabe, Masakazu Takayasu, Niwa, Aichi, Osuka, Koji, Nakura, Takahiro, Matsuo, Naoki, Watabe, Takeya, and Takayasu, Masakazu
- Subjects
INTERLEUKIN-6 ,MONOCYTE chemotactic factor ,CHEMOKINES ,MONOKINES ,INTERFERON gamma ,CEREBROSPINAL fluid ,SUBARACHNOID hemorrhage ,CYTOKINES ,GENE expression ,INFLAMMATORY mediators ,INTERLEUKINS ,DIAGNOSIS - Abstract
Background: Interleukin-6 (IL-6), an inflammatory cytokine, plays important roles in cerebrospinal fluid (CSF) after subarachnoid hemorrhage (SAH). Chemokines are chemoattractant cytokines that regulate trafficking of monocytes/macrophages and lymphocytes to sites of inflammation. However, no studies have been reported regarding the temporal expression of these cytokines in CSF after SAH.Findings: The concentrations of IL-6, monocyte chemoattractant protein-1 (MCP-1), interferon-γ-inducible protein-10 (IP-10), and monokine induced by interferon-γ (MIG) in the CSF of ten patients with SAH were measured using ELISA kits over a period of 14 days. All aneurysms were located in the anterior circulation. CSF samples from patients with unruptured aneurysms were used as controls. The concentration of IL-6 significantly increased during the acute stage of the disease. The concentration of MCP-1 increased from days 1 to 5, peaking on day 3, and decreased thereafter. The concentrations of IP-10 and MIG progressively increased, peaked on day 5, and then gradually decreased. There were strong correlations between the maximum levels of IL-6 and MCP-1 and IP-10 and MIG on day 5. The maximum level of IL-6 was much higher in poor outcome patients than in good outcome patients.Conclusions: The present investigation demonstrated that increases in IL-6 levels may induce the expression of MCP-1 in CSF after SAH, followed by increases in the expression of IP-10 and MIG. Dynamic changes in the levels of these cytokines may induce inflammation and may be closely associated with the development of delayed ischemic neurological deficits after SAH. [ABSTRACT FROM AUTHOR]- Published
- 2016
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