Mast Cells in Allergic and Inflammatory Diseases

Abstract

Mast cells are important in the development of allergic and anaphylactic reactions, but also in acquired and innate immunity. There is also increasing evidence that mast cells participate in inflammatory diseases, where they can be activated by non-allergic triggers, such as neuropeptides and cytokines, often having synergistic effects as in the case of substance P (SP) and IL-33. Secretion of vasoactive mediators, cytokines and proteinases contribute to the development of coronary artery disease (CAD), as well as to diet-induced obesity and the metabolic syndrome. Mast cells may be able to orchestrate such different biological processes through their ability to release pro-inflammatory mediators selectively without the degranulation typical of allergic reactions. Recent evidence suggests that mitochondrial uncoupling protein 2 (UCP2) and mitochondrial translocation regulate mast cell degranulation, but not selective mediator release. Better understanding of these two processes and how mast cells exert both immunostimulatory and immunosuppressive actions could lead to the development of inhibitors of release of specific mediators with novel therapeutic applications.

SG-HQ2 inhibits mast cell-mediated allergic inflammation through suppression of histamine release and pro-inflammatory cytokines

“…3 Mast cells play key roles in immunoglobulin E (IgE)-mediated allergic reactions through secretion of preformed or newly synthesized mediators such as histamine, lipidderived mediators, chemokines, cytokines, and growth factors. 4 The signaling pathway of mast cells triggered by antigen cross-linking of IgE bound to FceRI has been previously described. After stimulation of FceRI, it increases degranulation, production of lipid-derived mediators, and expression of cytokines.…”

Mast cell specific immunological biomarkers and metabolic syndrome among middle-aged and older Chinese adults

“…The mean and standard deviation (mean ± SD) of continuous and normal distributional variables and median and interquartile range of conof MCs in diet-induced obesity and diabetes, MCs inhibitory medications used in obesity and diabetes in experimental models offer hope to patients with these common chronic inflammatory diseases [19][20][21][22][23][24][25].…”

“…Some studies have suggested that MCs participate in the pathogenesis of inflammatory diseases such as cardiovascular diseases and metabolic disorders, MCs dysfunction has been viewed as the main offenders in some chronic inflammatory disorders, but the exact mechanisms of MCs in the pathogenesis of these diseases are not fully understood [19][20][21][22][23][24][25][26][27][28]. Participating of MCs in inflammatory diseases can be activated by non-allergic triggers, such as cytokines, often having synergistic effects among them [20]. Our study found that both plasma MCs proteases and IgE levels are significant risk factors for human pre-diabetes and diabetes mellitus [26,27].…”

“…MCs exert their physiological and pathological activities by releasing granules containing proteases including MCs specific chymase and tryptase [17,18]. Recent studies have revealed that chymase and tryptase directly participated in insulin resistance, cardiovascular diseases and metabolic disorders, although the mechanisms are not fully understood [19][20][21][22][23][24][25][26][27]. Data from animal models proved the direct participation approved by the Huzhou City Ethics Committee and all subjects gave written, informed consent prior to participating in the study.…”

Are mast cells important in diabetes?

“…In addition, in some studies, it has been reported that mast cells may prevent obesity and diabetes in experimental animal models [79]. Moreover, diabetes mellitus may present inhibition of mast cell activation, a decrease of leukocyte-endothelial cell interactions, reduced numbers of leukocytes in inflammatory sites, a decrease of microvascular responses to inflammatory compounds, including histamine, a reduction in protein loss, and a decrease of acute inflammatory reactions [80].…”