Abstract
Anaphylaxis is an acute and life-threatening systemic reaction. Food, drug, aero-allergen and insect sting are known to induce anaphylaxis. Mast cells and basophils are known to mediate Immunoglobulin E (IgE)-dependent anaphylaxis, while macrophages, neutrophils and basophils mediate non IgE-dependent anaphylaxis. Histone deacetylases (HDACs) play various roles in biological processes by deacetylating histones and non-histones proteins. HDAC inhibitors can increase the acetylation of target proteins and affect various inflammatory diseases such as cancers and allergic diseases. HDAC3, a class I HDAC, is known to act as epigenetic and transcriptional regulators. It has been shown that HDAC3 can interact with the high-affinity Immunoglobulin E receptor (FcεRI), to mediate passive anaphylaxis and cellular interactions during passive anaphylaxis. Effects of HDAC3 on anaphylaxis, cellular interactions involving mast cells and macrophages during anaphylaxis, and any tumorigenic potential of cancer cells enhanced by mast cells will be discussed in this review. Roles of microRNAs that form negative feedback loops with hallmarks of anaphylaxis such as HDAC3 in anaphylaxis and cellular interactions will also be discussed. The roles of MCP1 regulated by HDAC3 in cellular interactions during anaphylaxis are discussed. Roles of exosomes in cellular interactions mediated by HDAC3 during anaphylaxis are also discussed. Thus, review might provide clues for development of drugs targeting passive anaphylaxis.
Highlights
Systemic anaphylaxis is an immediate acute reaction that is mediated by bioactive mediators, released mostly from mast cells [1,2]
The mast cell-specific knockout of Sirt1 shows increased mast cell activation both in vitro and in vivo [88,89]. These reports suggest that Histone deacetylases (HDACs) play important roles in allergies and anaphylaxis
We have shown that atopic dermatitis, passive cutaneous anaphylaxis (PCA) and passive systemic anaphylaxis (PSA) display common molecular features such as activation of FcεRI signaling, increased secretion of Th2 cytokines and increased amount of histamine released [60]
Summary
Systemic anaphylaxis is an immediate acute reaction that is mediated by bioactive mediators, released mostly from mast cells [1,2]. Hyaluronic acid can attenuate allergic skin inflammation [16] and decrease the expression level of HDAC3 [17] These reports suggest that HDACs play important roles in active and passive anaphylaxis. Mast cells express the high-affinity IgE receptor FcεRI and mediate IgE-dependent allergies and anaphylaxis, such as PCA and food-induced systemic anaphylaxis [2,6,26,27,28,29,30]. Glycomacropeptide (GMP), a novel inhibitor of anaphylaxis, can increase the production of TGFβ1, attenuate mast cell activation by allergen, and suppress the secretion of histamine in the rat model of anaphylaxis [59] These reports suggest that PSA mediated by IgE is closely associated with suppression of functions of FOXP3+ Tregs. The nuclear receptor corepressor SMRT can enhance the deacetylase activity of HDAC3 toward MEF2 [74]
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