Interplay between mast cells and hormones: Part 2 of 8

Hormone Location released Major functions Interaction with mast cells Reference
Beta endorphin Pituitary Inhibits pain signaling In two studies, beta endorphin was shown to induce histamine release from mast cells; however, this phenomenon has not been seen by other researchers.

Sensation of pain activates mast cells and can also trigger endorphin release, so interplay between endorphins and mast cells is possible.

Kimura T, et al. Intradermal application of nociception increases vascular permeability in rats: the possible involvement of histamine release from mast cells. European Journal of Pharmacology 2000: 407, 327-332.
Brain natriuretic peptide (BNP) Heart Reduce systemic vascular resistance and water, sodium and fat in blood, decreasing blood pressure

Decrease cardiac output

Vasodilator

Relax smooth muscle of airway

BNP directly activates mast cells in a dose dependent fashion. Yoshida H, et al. Histamine release induced by human natriuretic peptide from rat peritoneal mast cells. Regulatory Peptides 1996: 61, 45-49.
Calcidiol/ Vitamin D3 (inactive) Skin Inactive form of vitamin D3 Vitamin D decreases IgE dependent mast cell activation and cytokine production in a dose dependent fashion.

 

 

Yip KH, et al. Mechanisms of vitamin D3 metabolite repression of IgE-dependent mast cell activation. Journal of Allergy and Clinical Immunology 2014: 133 (5), 1356-1364.
Calcitonin Thyroid Stimulates bone construction

Promotes retention of calcium in bone

One report in 1994 noted that serum calcitonin was increased in a patient with SM. Yocum MW, et al. Increased plasma calcitonin levels in systemic mast cell disease. Mayo Clin Proc 1994: 69 (10), 987-990.
Calcitriol/ Vitamin D3 Kidney Promote absorption of calcium and phosphate in GI tract

Inhibit release of parathyroid hormone in kidneys

Vitamin D decreases IgE dependent mast cell activation and cytokine production in a dose dependent fashion.

 

 

Yip KH, et al. Mechanisms of vitamin D3 metabolite repression of IgE-dependent mast cell activation. Journal of Allergy and Clinical Immunology 2014: 133 (5), 1356-1364.
Cholecystokinin Small intestine Release of digestive enzymes from pancreas and bile from gallbladder

Suppresses hunger

Stimulates vagus nerve

Decreases gastric emptying and GI motility

Unclear role in medication tolerance and withdrawal

The form of CCK most predominant in intestine (CCK-33) stabilizes mast cells.

May have a role in preventing mast cell degranulation as a response to food.

Vergara P, et al. Neuroendocrine control of intestinal mucosal mast cells under physiological conditions. Neurogastroenterology 2002: 14(1), 35-42.
Corticotropin releasing hormone (CRH) Hypothalamus Stimulate ACTH release from pituitary CRH binds to mast cell receptors CRHR-1 and CRHR-2 causing release of VEGF but not histamine, tryptase or IL-8.

CRH is also released by mast cells.

Theoharides TC, et al. Mast cells and inflammation. Biochim Biophys Acta 2012: 1822(1), 21-33.
Cortisol and other glucocorticoids Adrenal gland (cortex) Breaks down fat in adipose tissue

Drives production of glucose, epinephrine and norepinephrine

Inhibits immune action and inflammation, protein production, and glucose transfer to muscle and adipose tissue

Cortisol has a wide range of other effects

Glucocorticoids inhibit mediator production in several ways.

Decreases prostaglandin production by decreasing levels of COX-2, an enzyme that makes prostaglandins.

Decreases production of leukotrienes, prostaglandins and thromboxanes by increasing anti-inflammatory molecules.

Triggers release of annexin-1, an anti-inflammatory molecule that is also involved in the mast cell stabilizing mechanism of cromolyn.

Lowers bradykinin levels, decreasing swelling.

Directly interferes with production and secretion of cytokines.

The role of Annexin-A1/FPR2 system in the regulation of mast cell degranulation provoked by compound 48/80 and in the inhibitory action of nedocromil. International Immunopharmacology 2016: 32, 87-95.

Oppong E, et al. Molecular mechanisms of glucocorticoid action in mast cells. Mol Cell Endocrinol 2013: 380, 119-126.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Author’s note: I tried to hit the high notes here but cortisol has a massive range of effects on immune function, including mast cells, so the next post in this series will be dedicated just to cortisol and the effects on mast cells.

 

 

 

 

3 Responses

  1. henry rose June 14, 2016 / 6:03 pm

    hi , i am amazed the work that you are doing , the dept of associating all the scientific evidence is going to be the way to find some kind of solution or adjustment . my wife has systemic masto cytosis and is in an advance stage. i can’t relate to all the scientific information but in a total system i see the relation my wive side effect are correlating to the evidence you have complied. you are doing great job , may god give you strength .
    henry rose , harose@yahoo.com , you can contact me any time 818-207-9117

  2. becca June 15, 2016 / 8:13 am

    Useful information. For your question pot:
    Please forgive this if you’ve addressed it elsewhere as you probably have, but what’s the difference between “activation” and “degranulation?”
    May I also suggest a thought experiment? I’d like to know your ideas. The species (as well as any animals with collagen and mast cells) passes on EDS and mast cell disorders; individuals may suffer, but live to reproduce and perpetuate the genes. Could there actually be some advantages? what would they be?
    I’m thinking along the lines of the theory that there’s protection from malaria in sickle cell.
    Thanks, Becca

    • Lisa Klimas June 15, 2016 / 9:01 pm

      If I were to expect an evolutionary benefit to mast cell disease, I would expect that it conferred strong resistance to GI parasites or ability to heal wounds quickly.

      Mast cell activation refers to an inflammatory state triggered in mast cells. Depending upon how the cells are activated (in response to what/what receptor/where in the body), mast cells can do a few things. The first is degranulation, release of already made mediators that are sitting in bubbles (granules) inside mast cells. Some activation pathways will trigger full degranulation (release entire contents of granules at once). Others will trigger piecemeal degranulation (release some contents of granules). Still others will induce mast cells to make new mediators and then secrete them right away instead of storing them in granules.

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