D3.346 - Impact of local craniocerebral hypothermia on inflammatory cytokine production in ischemic stroke
Background
Multiple pathophysiologic changes after ischemic stroke induce neuroinflammation, abnormal activation of immune cells, and neuronal death. Inflammatory responses due to increased production of proinflammatory cytokines, chemokines and adhesion molecules are key factors of ischemic tissue damage including progression of ischemic stroke. Therapeutic approaches to reduce the activity of inflammatory cytokines may become key to suppressing inflammatory processes that occur during ischemic stroke. Local craniocerebral hypothermia (LCCH) may suppress inflammation in patients with acute cerebrovascular disorders. This study investigates the impact of LCСH on the production of inflammatory cytokines.
Method
The study included 18 patients with acute cerebrovascular accident consistent with the diagnosis of ischemic stroke. The main group included 16 patients who underwent LCCH sessions along with standard basic therapy. The control group (n=20) received only the standard basic therapy. Pro-inflammatory cytokines (IL-6, TNFa and IL-1a) in blood plasma of patients were assessed by ELISA using test KITs (RayBiotech, USA) on the immune analyzer ANTHOS 2010 (Anthos Labtec Instruments GmbH, Austria).
Results
The investigation demonstrated an increase in all studied cytokines compared to reference values in ischemic stroke patients. IL-6 showed a more pronounced increase (23.12+ 2.41 ng/ml) than other cytokines. The concentrations of Il-1a was 12.10 ± 3.18 ng/ml and TNFa was 7.54 ± 2.45 ng/ml, respectively. After LCCH sessions along with standard basic therapy there was a decrease in the concentration of the studied pro-inflammatory cytokines by 2.3 fold for IL-6; 1.68 fold for Il-1a; and 1.76 fold for TNFa, respectively. There was a less pronounced (p=0.05) decrease in all the cytokines of the control group treated with standard therapy without LCCH.
Conclusion
LCCH therapy added to standard basic therapy for ischemic stroke may induce a more pronounced decrease in the concentration of major proinflammatory cytokines compared to the effect of standard basic therapy for ischemic stroke.
