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Central nervous system administration of interleukin-6 produces splenic sympathoexcitation

Bryan G Helwig1, Robin A Craig1, Richard J Fels1

  • 1Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506, United States.

Autonomic Neuroscience : Basic & Clinical
|June 13, 2008
PubMed

Insights

Interleukin-6 (IL-6) administered into the brain ventricles increases sympathetic nerve activity. This cytokine acts in periventricular areas, not throughout the brain parenchyma, to influence sympathetic outflow.

Area of Science:

  • Neuroimmunology
  • Autonomic Nervous System Regulation
  • Cytokine Signaling

Background:

  • Interleukin-6 (IL-6) is a key cytokine involved in central physiological responses, including the hypothalamic-pituitary-adrenal axis.
  • Elevated cerebrospinal fluid (CSF) IL-6 levels are observed in conditions like Alzheimer's disease, autoimmune disorders, and meningitis.
  • The impact of IL-6 on the central regulation of sympathetic nerve discharge (SND) is not well understood, limiting insights into sympathetic-immune interactions.

Purpose of the Study:

  • To investigate the effect of intracerebroventricular (i.c.v.) administration of IL-6 on splenic SND in rats.
  • To determine if i.c.v. administered IL-6 penetrates the brain parenchyma and influences areas regulating sympathetic nerve outflow via volume transmission.

Main Methods:

  • Rats were anesthetized with urethane-chloralose.
  • Splenic SND was measured following i.c.v. injection of varying doses of IL-6 (10 ng, 100 ng, 400 ng) in baroreceptor-denervated Sprague-Dawley rats.
  • Distribution of fluorescently labeled IL-6 and co-localization with the IL-6 receptor (IL-6R) in brain tissue was assessed 60 minutes post-injection.

Main Results:

  • I.c.v. administration of IL-6 dose-dependently and significantly increased splenic SND.
  • Higher doses of IL-6 (100 ng and 400 ng) produced significantly greater SND responses compared to the 10-ng dose.
  • Fluorescently labeled IL-6 was localized to periventricular areas of the ventricular system, not distributed throughout the brain parenchyma.
  • IL-6 and IL-6R were co-localized in periventricular regions adjacent to the third ventricle.

Conclusions:

  • Intracerebroventricular IL-6 administration effectively increases splenic sympathetic nerve discharge.
  • The effects of i.c.v. IL-6 on SND appear to be mediated by signaling within periventricular cells, rather than widespread parenchymal action.
  • These findings highlight a mechanism for IL-6 in regulating autonomic function via periventricular pathways.

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