Journal
JOURNAL OF NEUROIMMUNOLOGY
Volume 193, Issue 1-2, Pages 130-139Publisher
ELSEVIER
DOI: 10.1016/j.jneuroim.2007.10.029
Keywords
neuronal nicotinic; lnflammation; ultraviolet radiation; cytokine; SOCS3
Categories
Funding
- NHLBI NIH HHS [P01 HL072903-059001, P01 HL072903, P01 HL72903] Funding Source: Medline
- NIA NIH HHS [R01 AG029838] Funding Source: Medline
- NIDA NIH HHS [R01 DA025057, R01 DA015148-04, DA018930, DA015148, R01 DA015148, R21 DA018930, R21 DA018930-02] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P01HL072903] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG029838] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA015148, R21DA018930, R01DA025057] Funding Source: NIH RePORTER
Ask authors/readers for more resources
The anti-inflammatory effects of the neuronal nicotinic receptor alpha7 (nAChR alpha 7) 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 naAChR agonist, were reduced. Conversely, nAChR alpha 7 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 nAChR alpha 7 can participate in modulating a local pro-inflammatory response in the absence of parasympathetic innervation. (C) 2007 Elsevier B.V. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available