Increase in Activity of Neutrophils and Proinflammatory Mediators in Rats Following Acute and Prolonged Focal Cerebral I
It has been proposed that the immune system is activated during ischemic cerebral events and that brain damage caused by ischemia is increased by this immune activity. Neutrophils (PMNs) are one of the first factors in the chain of reactions of the immune
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ract Purpose It has been proposed that the immune system is activated during ischemic cerebral events and that brain damage caused by ischemia is increased by this immune activity. Neutrophils (PMNs) are one of the first factors in the chain of reactions of the immune system during focal cerebral ischemia. Experimental and clinical studies have emphasized the important role of proinflammatory cytokines such as interleukin-1b (IL-1b) and tumor necrosis factor (TNFa), in addition to vasoactive peptide and endothelin-1 (ET-1), in the formation of cerebral ischemia. Material and Methods The experiments were carried out using Wistar rats that were divided into four groups: three experimental groups (acute and prolonged focal cerebral ischemia and following reperfusion) and one control group (sham). Focal cerebral ischemia was induced by the intraluminal surgical suture method. The oxidative activity of PMNs was measured after stimulation with phorbol myristate acetate, a protein kinase C activator (luminol enhanced chemiluminescence). The concentration of IL-1b and TNFa in rat lymphocyte culture after stimulation with CSF was determined using commercial ELISA kits. The plasma concentration of ET-1 was determined using commercial kits with the RIA method. Results We confirmed a statistically significant increase in the oxidative activity of PMNs in rats with acute focal cerebral ischemia (p < 0.00001), prolonged ischemia (p < 0.001) and reperfusion (p < 0.05). An increase in IL-1b and TNFa in lymS. Hendryk (*), P. Baz˙owski, and H. Dolez˙ych Department of Neurosurgery, Medical University of Silesia, Katowice, Medyków 14 street, 40-752, Katowice, Poland e-mail: [email protected] Z. Czuba and W. Król Department of Microbiology and Immunology in Zabrze, Medical University of Silesia, Jordana 19 street, 41-808 Zabrze-Rokitnica, Poland H. Jędrzejewska-Szypułka Department of Physiology, Medical University of Silesia, Katowice, Medyków 18 street, 40-752, Katowice, Poland
phocytes following CSF stimulation was observed in the group with prolonged ischemia and in the group with reperfusion after transient ischemia (p < 0.05 for both). An increase in plasma ET-1 concentration was observed with acute and prolonged focal cerebral ischemia (p < 0.05 and p < 0.01, respectively). Conclusions Our results show that acute and prolonged focal cerebral ischemia and reperfusion induce statistically significant increases in the oxidative activity of PMNs. The concentration of proinflammatory mediators (IL-1b, TNFa) as well as ET-1 is also increased, indicating the important role of immune reactions in the development of damage to the brain following ischemia. Keywords Focal cerebral ischemia–reperfusion • neutrophils • proinflammatory mediators
Introduction Interleukin-1 (IL-1) is a key mediator of inflammation during cerebral ischemia, but its precise mechanisms of action remain unclear (42). It is known that free radicals and inflammatory mediators are involved in transient focal cerebral ischemia, and Khan et al. (29) demonstrat
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