Nicotinic acetylcholine receptor α7 subunit is an essential regulator of inflammation

By Hong Wang, Man Yu, M. Ochani, C. Amella, Mahira Tanović, Seenu M. Susarla, J. Li, Haichao Wang, Huan Yang, Luis Ulloa and 3 more. Nature, 2002

2,872 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/e50736dcca460c3212e3dedde319cc5876230f52

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Citations in the corpus

Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemia (2008, background): “In vitro, acetylcholine and other cholinergic agonists attenuate LPSinduced TNF in human and mouse macrophages and in mouse splenocytes through an 7-dependent mechanism (2, 4).”
Acetylcholine beyond neurons: the non‐neuronal cholinergic system in humans (2008, neutral): “…Kawashima and Fujii (2003) (B, F, R); (39) Kawashima et al. (2007) (R); (40) Reinheimer et al. (2000) (F); (41) Profita et al. (2005) (F, I); (42) Wang et al. (2003) (F, KO, R); (43) Blanchet et al. (2007) (F, I, R); (44) Qu et al. (2006) (R); (45) Roman et al. (2004) (F); (46) Sekhon et al.…”
Sepsis: current dogma and new perspectives. (2014, background): “…or splenic nerves, genetically ablating a7nAChR, or pharmacologically inhibiting signals along this pathway all enhance cytokine release and the increase the severity of of lethal shock and tissue injury (Bernik et al., 2002; Borovikova et al., 2000; Rosas-Ballina et al., 2008; Wang et al., 2003).”
The Cholinergic Anti-inflammatory Pathway: A Missing Link in Neuroimmunomodulation (2003, background): “The nicotinic acetylcholine receptor α7 subunit is essential for regulation of peripheral inflammatory responses; activation of this receptor via vagus nerve stimulation (105) or cholinergic agonists (119,120) suppresses cytokine release and protects against lethal murine endotoxemia and sepsis.”
Mammalian Nicotinic Acetylcholine Receptors: From Structure to Function (2009, background): “Recent studies of mice suggest that this may in part be related to specific nAChRs and their interactions with distinct inflammatory pathways (353, 366, 489), which in turn are subject to individual genetics.”