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Inhibitory role of cholinergic system mediated via alpha7 nicotinic acetylcholine receptor in LPS-in

Discussion in 'Other Health News and Research' started by lansbergen, Dec 27, 2012.

  1. lansbergen

    lansbergen Senior Member

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  2. lansbergen

    lansbergen Senior Member

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    Journal of Experimental Pharmacology

    https://www.dovepress.com/getfile.php?fileID=5437

    Functional role of the nicotinic arm of the acetylcholine regulatory axis in human B-cell lines

    Juan Arredondo1 Denys Omelchenko2 Alexander I Chernyavsky1 Jing Qian1
    Maryna Skok2 Sergei A Grando1

    1Institute for Immunology and Departments of Dermatology and Biological Chemistry, University of California, Irvine, CA, USA;
    2Palladin Institute of Biochemistry, Kiev, Ukraine

    Abstract: We studied the involvement of nicotinic acetylcholine receptors (nAChRs) in the
    inflammation-related activity of human B-cell lines. Activation of nAChRs in Daudi cells with
    epibatidine abolished the pansorbin-dependent upregulation of the pro-inflammatory marker
    Cox-2 both at the mRNA and protein levels, indicating that the nicotinergic signaling suppresses
    B-cell activation. While the anti-inflammatory action on B-cells was mediated predominantly
    through α7 nAChR, as could be judged from abolishing epibatidine effects with methyllycaconitine,
    both α7 and non-α7 nAChRs, such as α2-containing receptors, were involved in regulation of B-cell apoptosis.
    The net effect was antiapoptotic. To determine the role of nAChRs
    in regulating B-cell activation/plasmacytic differentiation, we measured changes in the CD38,
    CD138 and Bcl-6 gene expression. Epibatidine significantly (P  0.05) upregulated CD38 at the
    transcriptional level and CD138 and Bcl-6 – at the translational levels. AR-R17779 significantly
    (P  0.05) increased the protein levels of CD38 and CD138. In both cases, the effect of epibatidine
    was abolished with Mec, and that of AR-R17779 – by MLA, demonstrating a functional
    role of nAChRs in regulating Daudi cell differentiation. The obtained results revealed distinct
    contributions of α7 and non-α7 nAChRs to regulation of B-cell activation/differentiation, and
    suggested that signaling through the nicotinic arm of acetylcholine regulatory axis is important
    for B-cell involvement in inflammation.
  3. blue sky

    blue sky

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    southwest USA
    Not sure if it is activating the same receptors as what is being discussed, but there is an anti-inflamatory product made from tobacco that inhibits NFkb. It's called anatabine (sold as Anatabloc). Note that it does contain vitamin A and D in the formulation (just a caution for those who are intolerant to those types of ingredients). It is also considered in the same family as "nightshades", which may be problematic for some.

    The website is www.anatabloc.com/home
    I was told about this supplement (no script required) by the nurse practitioner that I am seeing for me/cfs (and lyme dx recently). She reported that her sister works for a tobacco company, and they had some studies showing it was a powerful anti-inflamatory. I ran across some testimonials, one of which was someone who identified himself as having cfs and reported that he was much improved (I believe he wrote that he was back to normal, if my memory serves me). Unfortunately, I haven't yet had time to look into this more, but thought it might be relevant to this topic.

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