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      Impact of Capsaicin on Mast Cell Inflammation

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          Abstract

          Mast cells are inflammatory cells, and they are prominent in inflammatory diseases such as allergy and asthma. Mast cells possess high-affinity receptors for IgE (FCεRI) and the cross-linking of these receptors is essential to trigger the secretion of granules containing arachidonic acid metabolism [such as prostaglandin (PG) D2, leukotriene (LT) B4, and LTC4], histamine, cytokines, chemokines, and proteases, including mast cell-specific chymases and tryptases. Activation of mast cells provokes the secretion of cytokines and mediators that are responsible for the pathologic reaction of immediate hypersensitivity. Sensory nerve stimulation by irritants and other inflammatory mediators provokes the release of neuropeptides, causing an increase in vascular permeability, plasma extravasation and edema. Trigeminal nerve stimulation actives dura mast cells and increases vascular permeability, effects inhibited by capsaicin. Capsaicin causes release of sensory neuropeptide, catecholamines and vasodilation. Several studies have reported that capsaicin is effective in relief and prevention of migraine headaches, improves digestion, helps to prevent heart disease, and lowers blood cholesterol and blood pressure levels. The findings reported in these studies may have implications for the pathophysiology and possible therapy of neuroinflammatory disorders.

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          Differential release of mast cell mediators and the pathogenesis of inflammation.

          Mast cells are well known for their involvement in allergic and anaphylactic reactions, during which immunoglobulin E (IgE) receptor (Fc epsilon RI) aggregation leads to exocytosis of the content of secretory granules (1000 nm), commonly known as degranulation, and secretion of multiple mediators. Recent findings implicate mast cells also in inflammatory diseases, such as multiple sclerosis, where mast cells appear to be intact by light microscopy. Mast cells can be activated by bacterial or viral antigens, cytokines, growth factors, and hormones, leading to differential release of distinct mediators without degranulation. This process appears to involve de novo synthesis of mediators, such as interleukin-6 and vascular endothelial growth factor, with release through secretory vesicles (50 nm), similar to those in synaptic transmission. Moreover, the signal transduction steps necessary for this process appear to be largely distinct from those known in Fc epsilon RI-dependent degranulation. How these differential mast cell responses are controlled is still unresolved. No clinically available pharmacological agents can inhibit either degranulation or mast cell mediator release. Understanding this process could help develop mast cell inhibitors of selective mediator release with novel therapeutic applications.
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            Author and article information

            Journal
            International Journal of Immunopathology and Pharmacology
            Int J Immunopathol Pharmacol
            SAGE Publications
            2058-7384
            2058-7384
            July 2013
            July 01 2013
            July 2013
            : 26
            : 3
            : 597-600
            Affiliations
            [1 ] Parasitology Department, Veterinary School, Thessaloniki University, Greece
            [2 ] Dental School, University of Chieti-Pescara, Italy
            [3 ] Department of Dermatology, University of Rome Tor Vergata, Rome, Italy
            [4 ] Orthopeadics Division, University of Perugia, Italy
            [5 ] Gynecology Clinic, Pescara Hospital, Pescara, Italy
            [6 ] Surgery Division, Ortona Hospital, Ortona, Italy
            [7 ] Immunology Division, Medical School, University of Chieti-Pescara, Italy
            [8 ] Department of Human Movement Science, University of Chieti-Pescara, Chieti, Italy
            [9 ] Orthopedic Division, University of Chieti-Pescara, Italy
            [10 ] Department of Neuroscience and Imaging, University of Chieti-Pescara, Italy
            [11 ] Laboratory Medicine, University of Chieti-Pescara, Italy
            [12 ] Department of Pharmacology and Experimental Therapeutics, Biochemistry and Internal Medicine Tufts University School of Medicine, Tufts-New England Medical Center, Boston, MA, USA
            [13 ] Department of Internal Medicine, Catholic University of the Sacred Heart, Rome, Italy
            Article
            10.1177/039463201302600303
            24067456
            f90fcff0-3f91-4487-8d2d-f83d3be72aea
            © 2013

            http://journals.sagepub.com/page/policies/text-and-data-mining-license

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