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Clearance of ¹²⁵I-Labeled Interleukin-6 from Brain into Blood Following Intracerebroventricular Injection in Rats¹

Department of Medicine (G.C., W.L.C., S.R.), University of Arizona College of Medicine, Tucson, Arizona 85724; Department of Pharmacy Practice and Science (H.-H.C.), University of Arizona College of Pharmacy, Tucson, Arizona 85721; and Enid and Mel Zuckerman Fellow in Psychoneuroimmunology (W.L.C.), Arthritis Division, University of Arizona College of Medicine, Tucson, Arizona 85724

Address all correspondence and requests for reprints to: Seymour Reichlin, University of Arizona College of Medicine, Department of Medicine, Arizona Health Sciences Center, Room 7338, 1501 North Campbell Avenue, Box 245021, Tucson, Arizona 85724-5021. E-mail: reichlin{at}u.arizona.edu

To test the hypothesis that interleukin-6 (IL-6) induced within the brain can be released into peripheral blood, ¹²⁵I-labeled IL-6 was injected into the lateral cerebral ventricle of rats, and its concentration in peripheral blood followed serially. Acid-precipitable tracer appeared within 5 min of injection and entered the blood following first-order kinetics (fractional rate, 0.0116 ± 0.0022/min). Comparison of areas under the curve of intracerebroventricular (icv) vs. iv injection showed that 37.1–46.5% of tracer injected into the lateral cerebral ventricle appeared in the blood over a 4-h period. icv IL-6 exits at least in part via venous drainage (superior sagittal sinus/aortic concentration gradient was 1.47 ± 0.23 and 3.05 ± 0.87 in two separate groups). Prior icv injection of human IL-1ß (100 ng) did not alter rate of degradation or of exit of radioiodine-labeled IL-6 from the brain. These studies indicate that a relatively high proportion of IL-6 that arises in the brain enters the peripheral circulation. Direct secretion of IL-6 from brain to blood may be a mechanism by which the brain modifies peripheral metabolic, endocrine, and immune activity.

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