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Response to Bernardo de La Paz (Reply #2)

Thu Apr 23, 2020, 05:33 PM

33. You might have figured this out

Nicotine is a nonselective agonist of the α7Ach receptor and is able to suppress the production of proinflammatory cytokines by mimicking the binding of acetylcholine. It has been demonstrated that nicotine can selectively reduce the inflammatory response in a number of infection scenarios, including Legionella pneumophila (54) and Chlamydia pneumoniae (55) infection; however, it is highly unlikely that nicotine will ever be used clinically due to its toxicity, addictive nature, and lack of specificity.


From Clin Vaccine Immunol. 2013 Mar; 20(3): 319–327.
doi: 10.1128/CVI.00636-12
PMCID: PMC3592351
PMID: 23283640
Targeting the “Cytokine Storm” for Therapeutic Benefit
Riccardo V. D'Elia,corresponding author Kate Harrison, Petra C. Oyston, Roman A. Lukaszewski, and Graeme C. Clark

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3592351/

There's also a paper about the use of nicotine to suppress cytokine production in Crohn's Disease:

In-vivo effect of nicotine on cytokine production by human non-adherent mononuclear cells. (result: Nicotine inhibits Interleukin 10)

https://www.ncbi.nlm.nih.gov/pubmed/8930570

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