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Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation.
Nature. 2003 Jan 23; 421(6921):384-8.Nat

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 disease. 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 responses. This physiological mechanism, termed the 'cholinergic anti-inflammatory pathway' 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 alpha7 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 alpha7-deficient mice. Thus, the nicotinic acetylcholine receptor alpha7 subunit is essential for inhibiting cytokine synthesis by the cholinergic anti-inflammatory pathway.

Authors+Show Affiliations

Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute, 350 Community Drive, Manhasset, New York 11030, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12508119

Citation

Wang, Hong, et al. "Nicotinic Acetylcholine Receptor Alpha7 Subunit Is an Essential Regulator of Inflammation." Nature, vol. 421, no. 6921, 2003, pp. 384-8.
Wang H, Yu M, Ochani M, et al. Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. Nature. 2003;421(6921):384-8.
Wang, H., Yu, M., Ochani, M., Amella, C. A., Tanovic, M., Susarla, S., Li, J. H., Wang, H., Yang, H., Ulloa, L., Al-Abed, Y., Czura, C. J., & Tracey, K. J. (2003). Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. Nature, 421(6921), 384-8.
Wang H, et al. Nicotinic Acetylcholine Receptor Alpha7 Subunit Is an Essential Regulator of Inflammation. Nature. 2003 Jan 23;421(6921):384-8. PubMed PMID: 12508119.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. AU - Wang,Hong, AU - Yu,Man, AU - Ochani,Mahendar, AU - Amella,Carol Ann, AU - Tanovic,Mahira, AU - Susarla,Seenu, AU - Li,Jian Hua, AU - Wang,Haichao, AU - Yang,Huan, AU - Ulloa,Luis, AU - Al-Abed,Yousef, AU - Czura,Christopher J, AU - Tracey,Kevin J, Y1 - 2002/12/22/ PY - 2002/10/31/received PY - 2002/12/02/accepted PY - 2003/1/1/pubmed PY - 2003/3/8/medline PY - 2003/1/1/entrez SP - 384 EP - 8 JF - Nature JO - Nature VL - 421 IS - 6921 N2 - Excessive inflammation and tumour-necrosis factor (TNF) synthesis cause morbidity and mortality in diverse human diseases including endotoxaemia, sepsis, rheumatoid arthritis and inflammatory bowel disease. 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 responses. This physiological mechanism, termed the 'cholinergic anti-inflammatory pathway' 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 alpha7 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 alpha7-deficient mice. Thus, the nicotinic acetylcholine receptor alpha7 subunit is essential for inhibiting cytokine synthesis by the cholinergic anti-inflammatory pathway. SN - 0028-0836 UR - https://www.unboundmedicine.com/medline/citation/12508119/Nicotinic_acetylcholine_receptor_alpha7_subunit_is_an_essential_regulator_of_inflammation_ L2 - https://doi.org/10.1038/nature01339 DB - PRIME DP - Unbound Medicine ER -