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Lessons from ME/CFS: Finding Meaning in the Suffering
If you're aware of my previous articles here at Phoenix Rising then it's pretty clear that I don't generally spend my time musing upon the philosophy of the disease. I find it better to spend my time reading research and trying my best to break it down to its core elements and write...
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Neurotensin and CRH Interactions Augment Human Mast Cell Activation

Discussion in 'Mast Cell Disorders/Mastocytosis' started by nanonug, Nov 17, 2012.

  1. nanonug

    nanonug Senior Member

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    Virginia, USA
    (This could be an explanation for Post-exertional Malaise seen from the perspective of Mast Cell Activation)


    1. PLoS One. 2012;7(11):e48934. doi: 10.1371/journal.pone.0048934. Epub 2012 Nov 14.

    Neurotensin and CRH Interactions Augment Human Mast Cell Activation.

    Alysandratos KD, Asadi S, Angelidou A, Zhang B, Sismanopoulos N, Yang H,
    Critchfield A, Theoharides TC.

    Molecular Immunopharmacology and Drug Discovery Laboratory, Department of
    Molecular Physiology and Pharmacology, Tufts University School of Medicine,
    Boston, Massachusetts, United States of America ; Allergy Clinical Research
    Center, Allergy Section, Attikon General Hospital, University of Athens Medical
    School, Athens, Greece ; Sackler School of Graduate Biomedical Sciences, Tufts
    University, Boston, Massachusetts, United States of America.

    Stress affects immunity, but the mechanism is not known. Neurotensin (NT) and
    corticotropin-releasing hormone (CRH) are secreted under stress in various
    tissues, and have immunomodulatory actions. We had previously shown that NT
    augments the ability of CRH to increase mast cell-dependent skin vascular
    permeability in rodents. Here we show that NT triggered human mast cell
    degranulation and significantly augmented CRH-induced vascular endothelial growth
    factor (VEGF) release. Investigation of various signaling molecules indicated
    that only NF-κB activation was involved. These effects were blocked by
    pretreatment with the NTR antagonist SR48692. NT induced expression of CRH
    receptor-1 (CRHR-1), as shown by Western blot and FACS analysis. Interestingly,
    CRH also induced NTR gene and protein expression. These results indicate unique
    interactions among NT, CRH, and mast cells that may contribute to auto-immune and
    inflammatory diseases that worsen with stress.

    PMID: 23155429
  2. magenk

    magenk

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    Do you know of any current studies involving neurotensin and mast cells? Article seems to indicate that reducing stress levels would be the best way to reduce MCAS.

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