Neuronal nicotinic alpha7 receptors modulate inflammatory cytokine production in the skin following ultraviolet radiation

Abstract The anti-inflammatory effects of the neuronal nicotinic receptor alpha7 (nAChRα7) are proposed to require acetylcholine release from vagal efferents. The necessity for vagal innervation in this anti-inflammatory pathway was tested in the skin, which lacks parasympathetic innervation, using...

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Bibliographic Details
Published in:Journal of neuroimmunology 2008-01, Vol.193 (1), p.130-139
Main Authors: Osborne-Hereford, Amber V, Rogers, Scott W, Gahring, Lorise C
Format: Article
Language:English
Subjects:
Allergy and Immunology
alpha7 Nicotinic Acetylcholine Receptor
Animals
Cytokine
Cytokines - biosynthesis
Female
Inflammation
Interleukin-1beta - biosynthesis
Interleukin-6 - biosynthesis
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Neurology
Neuronal nicotinic
Nicotine - pharmacology
Receptors, Nicotinic - physiology
Skin - immunology
Skin - pathology
Skin - radiation effects
SOCS3
Suppressor of Cytokine Signaling 3 Protein
Suppressor of Cytokine Signaling Proteins - physiology
Ultraviolet radiation
Ultraviolet Rays
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Summary:Abstract The anti-inflammatory effects of the neuronal nicotinic receptor alpha7 (nAChRα7) are proposed to require acetylcholine release from vagal efferents. The necessity for vagal innervation in this anti-inflammatory pathway was tested in the skin, which lacks parasympathetic innervation, using ultraviolet radiation (UVB) to induce a local pro-inflammatory response. Cytokine responses to UV in mice administered chronic oral nicotine, a nAChR agonist, were reduced. Conversely, nAChRα7 knock-out mice exposed to UVB elicit an enhanced pro-inflammatory cytokine response in the skin. Altered pro-inflammatory responses correlated with changes in SOCS3 protein. These results demonstrate that nAChRα7 can participate in modulating a local pro-inflammatory response in the absence of parasympathetic innervation.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2007.10.029