Nicotinic acetylcholine receptor α7 subunit is an essential regulator of inflammation

Hong Wang, Man Yu, Mahendar Ochani, Carol Ann Amella, Mahira Tanovic, Seenu Susarla, Jian Hua Li, Haichao Wang, Huan Yang, Luis Ulloa, Yousef Al-Abed, Christopher J. Czura and Kevin J. Tracey ()
Additional contact information
Hong Wang: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Man Yu: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Mahendar Ochani: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Carol Ann Amella: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Mahira Tanovic: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Seenu Susarla: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Jian Hua Li: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Haichao Wang: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Huan Yang: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Luis Ulloa: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Yousef Al-Abed: Laboratory of Medicinal Chemistry, North Shore Long Island Jewish Research Institute
Christopher J. Czura: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute
Kevin J. Tracey: Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute

Nature, 2003, vol. 421, issue 6921, 384-388

Abstract: Abstract Excessive inflammation and tumour-necrosis factor (TNF) synthesis cause morbidity and mortality in diverse human diseases including endotoxaemia, sepsis, rheumatoid arthritis and inflammatory bowel disease1,2,3,4. Highly conserved, endogenous mechanisms normally regulate the magnitude of innate immune responses and prevent excessive inflammation. The nervous system, through the vagus nerve, can inhibit significantly and rapidly the release of macrophage TNF, and attenuate systemic inflammatory responses5,6,7. This physiological mechanism, termed the ‘cholinergic anti-inflammatory pathway’5 has major implications in immunology and in therapeutics; however, the identity of the essential macrophage acetylcholine-mediated (cholinergic) receptor that responds to vagus nerve signals was previously unknown. Here we report that the nicotinic acetylcholine receptor α7 subunit is required for acetylcholine inhibition of macrophage TNF release. Electrical stimulation of the vagus nerve inhibits TNF synthesis in wild-type mice, but fails to inhibit TNF synthesis in α7-deficient mice. Thus, the nicotinic acetylcholine receptor α7 subunit is essential for inhibiting cytokine synthesis by the cholinergic anti-inflammatory pathway.

Date: 2003
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DOI: 10.1038/nature01339

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