Add like
Add dislike
Add to saved papers

Sympathetic inhibition of IL-6, IFN-γ, and KC/CXCL1 and sympathetic stimulation of TGF-β in spleen of early arthritic mice.

OBJECTIVES: The connection between sympathetic nerve fibers and immune cells in the spleen is known. In the context of arthritis, the functional meaning of the neuroimmune contact remains unclear. From immunization until disease outbreak, the sympathetic nervous system (SNS) has a proinflammatory influence which is converted into an anti-inflammatory influence after disease outbreak. This study investigated the influence of neuronally released neurotransmitters on IFN-γ, KC (CXCL1), IL-6, and TGF-β in spleen of mice shortly after outbreak of collagen type II-induced arthritis.

METHODS: Spleens were removed when animals reached an arthritis score of 3 on a scale of 1-16 (approx. on day 32) in order to generate 0.35 mm-thick spleen slices. Spleen slices were transferred to superfusion microchambers in order to electrically induce release of sympathetic neurotransmitters. By means of this technique, the effect of physiologically released neurotransmitters was investigated on secretion of IFN-γ, KC, IL-6, and TGF-β.

RESULTS: High amounts of IFN-γ, KC, IL-6, and TGF-β were released from superfused spleen, and electrical stimulation markedly inhibited IFN-γ, KC, and IL-6 release but pronouncedly stimulated TGF-β. The adrenergic influence via β-adrenoceptors stimulated release of IL-6 and, particularly, TGF-β. However, catecholamines inhibit release of IL-6 via α1-adrenergic pathways but without any effect on TGF-β. The co-transmitter adenosine stimulated IL-6 release via A1-adenosine receptors but no influence was recognized on TGF-β.

CONCLUSION: At disease outbreak, electrically released endogenous neurotransmitters of the SNS inhibit IFN-γ, KC, and IL-6 but β-adrenergically stimulate TGF-β. This creates an anti-inflammatory milieu that might be responsible for the observed dual influence of the SNS on arthritis.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app