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Abstract
Mast cells (MCs) have long been mainly regarded as effector cells in IgE-associated allergic disorders with potential immunoregulatory roles. Located close to the allergen entry sites in the skin and mucosa, MCs can capture foreign substances such as allergens, toxins, or noxious substances and are exposed to the danger signals produced by epithelial cells. MC reactivity shaped by tissue-specific factors is crucial for allergic responses ranging from local skin reactions to anaphylactic shock. Development of Th2 response leading to allergen-specific IgE production is a prerequisite for MC sensitization and induction of FcεRI-mediated MC degranulation. Up to now, IgE production has been mainly associated with proteins, whereas lipids present in plant pollen grains, mite fecal particles, insect venoms, or food have been largely overlooked regarding their immunostimulatory and immunomodulatory properties. Recent studies, however, have now demonstrated that lipids affect the sensitization process by modulating innate immune responses of epithelial cells, dendritic cells, and NK-T cells and thus crucially contribute to the outcome of sensitization. Whether and how lipids affect also MC effector functions in allergic reactions has not yet been fully clarified. Here, we discuss how lipids can affect MC responses in the context of allergic inflammation. Direct effects of immunomodulatory lipids on MC degranulation, changes in local lipid composition induced by allergens themselves and changes in lipid transport affecting MC reactivity are possible mechanisms by which the function of MC might be modulated.
Highlights
Mast cells are long-living tissue-resident hematopoietic cells equipped with secretory granules containing a broad spectrum of biologically active mediators such as histamine, proteases, and cytokines [1, 2]
Airway inflammation, mucus production, and airway hyperresponsiveness in vivo as well as Mast cells (MCs) degranulation and cytokine release were decreased by lipoxin B4 application [16], indicating therapeutic potential of pro-resolving lipid mediators in regulation of MC reactivity
Modulation of MC degranulation by affecting the lipid composition of the cell membrane or the enzyme activity modulating the lipid distribution of the membrane are potential emerging therapeutic strategies for the treatment of allergic diseases
Summary
Mast cells are long-living tissue-resident hematopoietic cells equipped with secretory granules containing a broad spectrum of biologically active mediators such as histamine, proteases, and cytokines [1, 2]. Enhanced reactivity of MCs could be the result of a combined action of allergen-lipid complexes and pro-allergic inflammatory mediators produced by epithelial cells (Figure 1). The epithelial cell-derived resolvins D1, D2, and lipoxin A4 have been found to suppress IgE-mediated histamine release from MCs via G-protein-coupled receptors [65].
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