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Abstract
Mast cells play a key role in the regulation of innate and adaptive immunity and are involved in pathogenesis of many inflammatory and allergic diseases. The most studied mechanism of mast cell activation is mediated by the interaction of antigens with immunoglobulin E (IgE) and a subsequent binding with the high-affinity receptor Fc epsilon RI (FcεRI). Increasing evidences indicated that mitochondria are actively involved in the FcεRI-dependent activation of this type of cells. Here, we discuss changes in energy metabolism and mitochondrial dynamics during IgE-antigen stimulation of mast cells. We reviewed the recent data with regards to the role played by mitochondrial membrane potential, mitochondrial calcium ions (Ca2+) influx and reactive oxygen species (ROS) in mast cell FcεRI-dependent activation. Additionally, in the present review we have discussed the crucial role played by the pyruvate dehydrogenase (PDH) complex, transcription factors signal transducer and activator of transcription 3 (STAT3) and microphthalmia-associated transcription factor (MITF) in the development and function of mast cells. These two transcription factors besides their nuclear localization were also found to translocate in to the mitochondria and functions as direct modulators of mitochondrial activity. Studying the role played by mast cell mitochondria following their activation is essential for expanding our basic knowledge about mast cell physiological functions and would help to design mitochondria-targeted anti-allergic and anti-inflammatory drugs.
Highlights
Mitochondria are semi-autonomous double-membrane-bound organelles of an endosymbiotic origin with various compartments for operating the metabolic reactions including the citric acid cycle, oxidative phosphorylation (OXPHOS) and fatty acid β-oxidation
The inhibited mitochondrial translocation might prevent the activation of calcium release-activated channels (CRAC) which plays a crucial role in Ca2+ from the extracellular environment indicates thattriclosan attenuates high-affinity immunoglobulin E (IgE) receptor (FcεRI)-dependent mast cell degranulation [18, 19]
Our previous data indicated that mitochondriatargeted antioxidant SkQ1 abrogates the antigen-dependent degranulation of rat basophilic leukemia (RBL-2H3) mast cells [67], which implies that mitochondrial reactive oxygen species (ROS) contribute to mast cell activation
Summary
Mitochondria are semi-autonomous double-membrane-bound organelles of an endosymbiotic origin with various compartments for operating the metabolic reactions including the citric acid cycle, oxidative phosphorylation (OXPHOS) and fatty acid β-oxidation. The antigen-dependent stimulation of mast cell was shown to effect the extracellular signal-regulated kinase (Erk1/2) dependent phosphorylation of mitochondrial STAT3 causing an increase in OXPHOS activity. The mitochondrial membrane potential (δ m) plays an important role in the regulation of FcεRI-mediated mast cell degranulation.
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