Nicotine May Help Asthma And Probably Other Inflammatory Conditions

Discussion in 'Scientific Studies' started by ecstatichamster, Aug 31, 2019.

  1. ecstatichamster

    ecstatichamster Member

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    nicotine in very small quantities inhibits the inflammatory leukotrenes. Cotinine found with nicotine in tobacco does not.

    Nicotine Inhibits FcεRI-Induced Cysteinyl Leukotrienes and Cytokine Production without Affecting Mast Cell Degranulation Through α7/α9/α10-Nicotinic Receptors

    Smokers are less likely to develop some inflammatory and allergic diseases. In Brown-Norway rats, nicotine inhibits several parameters of allergic asthma, including the production of Th2 cytokines and the cysteinyl leukotriene LTC4. Cysteinyl leukotrienes are primarily produced by mast cells, and these cells play a central role in allergic asthma. Mast cells express a high-affinity receptor for IgE (FcεRI). Following its cross-linking, cells degranulate and release preformed inflammatory mediators (early phase) and synthesize and secrete cytokines/chemokines and leukotrienes (late phase). The mechanism by which nicotine modulates mast cell activation is unclear. Using α-bungarotoxin binding and quantitative PCR and PCR product sequencing, we showed that the rat mast/basophil cell line RBL-2H3 expresses nicotinic acetylcholine receptors (nAChRs) α7, α9, and α10; exposure to exceedingly low concentrations of nicotine (nanomolar), but not the biologically inactive metabolite cotinine, for ≥8 h suppressed the late phase (leukotriene/cytokine production) but not degranulation (histamine and hexosaminidase release). These effects were unrelated to those of nicotine on intracellular free calcium concentration but were causally associated with the inhibition of cytosolic phospholipase A2 activity and the PI3K/ERK/NF-κB pathway, including phosphorylation of Akt and ERK and nuclear translocation of NF-κB. The suppressive effect of nicotine on the late-phase response was blocked by the α7/α9-nAChR antagonists methyllycaconitine and α-bungarotoxin, as well as by small interfering RNA knockdown of α7-, α9-, or α10-nAChRs, suggesting a functional interaction between α7-, α9-, and α10-nAChRs that might explain the response of RBL cells to nanomolar concentrations of nicotine. This “hybrid” receptor might serve as a target for novel antiallergic/antiasthmatic therapies.
     
  2. jamies33

    jamies33 Member

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    Haidut spoke on a podcast that nicotine may be useful, but promotes acetylcholine.

    Danny Roddy said that vaping has pro-inflammatory chemicals.

    The best dose seems to be gum, or patches? 1-2mg/day or so
     
  3. yerrag

    yerrag Member

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    I was on youtube and there's this guy who mentioned nicotine to be helpful against endotoxins but he was rattling off quickly so there was no specifics given. Wouldn't niacinamide be just as helpful?
     
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