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a Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Tufts–New England Medical Center, Boston, Massachusetts 02111, USA b Department of Biochemistry, Tufts University School of Medicine, Tufts–New England Medical Center, Boston, Massachusetts 02111, USA c Department of Internal Medicine, Tufts University School of Medicine, Tufts–New England Medical Center, Boston, Massachusetts 02111, USA d Allergy Division, Attikon Hospital, Athens University Medical School, Athens, Greece
Key Words: asthma • coronary artery disease • inflammation • dermatoses • mast cells • skin • stress • vascular permeability
Address for correspondence: T.C. Theoharides, Ph.D., M.D., Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA. Voice: 617-636-6866; fax: 617-636-2456. e-mail: theoharis.theoharides{at}tufts.edu
Mast cells are well known for their involvement in allergic and anaphylactic reactions, but recent findings implicate them in a variety of inflammatory diseases affecting different organs, including the heart, joints, lungs, and skin. In these cases, mast cells appear to be activated by triggers other than aggregation of their IgE receptors (Fc
 RI), such as anaphylatoxins, immunoglobulin-free light chains, superantigens, neuropeptides, and cytokines leading to selective release of mediators without degranulation. These findings could explain inflammatory diseases, such as asthma, atopic dermatitis, coronary inflammation, and inflammatory arthritis, all of which worsen by stress. It is proposed that the pathogenesis of these diseases involve mast cell activation by local release of corticotropin-releasing hormone (CRH) or related peptides. Combination of CRH receptor antagonists and mast cell inhibitors may present novel therapeutic interventions.
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