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Circulating Levels of Interleukin-10 and -17 in Patients with Cerebral Sinovenous Thrombosis (CSVT) in Acute and Subacute Stages: A Prospective Case-Control Study | ||
Iranian Journal of Immunology | ||
مقاله 6، دوره 15، شماره 3، آذر 2018، صفحه 221-227 اصل مقاله (124.91 K) | ||
نوع مقاله: Original Article | ||
شناسه دیجیتال (DOI): 10.22034/iji.2018.39391 | ||
نویسندگان | ||
Sadegh Izadi1؛ Afshin Borhani-Haghighi* 1؛ Kamal Bastani1؛ Bahareh Kardeh1؛ Golnaz Yadollahi-Khales2؛ Mojtaba Neydavoodi1 | ||
1Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran, | ||
2University of Illinois hospital, neurology department, Chicago, Illinois | ||
چکیده | ||
Background: Cerebral sinovenous thrombosis (CSVT) is a neurovascular disorder that occurs when a blood clot develops in a vein near the brain. Evaluating the subsequent changes in inflammatory cytokines can better reveal the underlying pathogeneses. Objective: To assess the serum levels of interleukin-10 (an anti-inflammatory cytokine) and IL-17 (a pro-inflammatory cytokine) in patients with aseptic non-vasculitic CSVT. Methods: In this prospective case-control study, 31 patients with aseptic non-vasculitic CSVT (admitted in Namazi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran) were enrolled. IL-10 and IL-17 serum levels were measured at diagnosis, before initiation of treatment (acute stage), 3 months later (subacute stage). These cytokines were also measured in samples obtained from 30 gender- and age-matched healthy subjects, which were considered as control values. Results: Patients’ IL-10 and IL-17 levels were higher in both acute and subacute stages as compared to controls. However, no significant differences existed between the acute stage and control groups for both cytokines. Moreover, subacute levels were significantly higher than their acute and control levels. Conclusion: This study demonstrated the alteration of IL-10 and IL-17 levels in aseptic non-vasculitic CSVT. The rise in subacute IL-10 can be explained by the assumption that IL-10 is released as an anti-inflammatory response to subside the effects of IL-17 mediated reactions. More importantly, the immediate sampling in the acute stage did not allow enough time for triggering the immune system to produce such mediators. However, a balance was established between IL-10 and IL-17 in the subacute stage to prevent further tissue damage. | ||
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