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Activation and Modulation of Mast Cells

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (31 December 2019) | Viewed by 53519

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Prof. Dr. Satoshi Tanaka

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Department of Pharmacology, Kyoto Pharmaceutical University, Misasagi Nakauchi-cho 5, Yamashina-ku, Kyoto 607-8414, Japan
Interests: mast cell; inflammation; degranulation; allergy; histamine; G protein-coupled receptor; IgE; cytokine

Special Issue Information

Dear Colleagues,

Accumulating evidence suggests that mast cells should be involved in a wide variety of inflammatory responses in addition to IgE-mediated immediate allergic responses. Mast cells were found to modulate cutaneous, bronchial, and intestinal inflammation in cooperation with dendritic cells, Th2 cells, Treg cells, and type 2 innate lymphoid cells. Mast cells could be novel therapeutic targets of various chronic inflammatory diseases, such as atopic dermatitis, asthma, and inflammatory bowel diseases, although it remains to be fully clarified how tissue mast cells are activated. Because all these inflammatory responses do not occur in the context of IgE, an understanding of the IgE-independent activation of mast cells should shed light on novel modulatory roles of tissue mast cells.

We warmly welcome original manuscripts and reviews dealing with the mechanism of the IgE-independent activation of mast cells, the characterization of tissue resident mast cells, and the modulation of mast cell activation.

Prof. Dr. Satoshi Tanaka
Guest Editor

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Keywords

mast cell
inflammation
G protein-coupled receptor (GPCR)
Mas-related G protein-coupled receptor (Mrgpr)
degranulation
immune tolerance
mast cell secretagogue
histamine
skin
gastrointestinal tract

Published Papers (12 papers)

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Editorial

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4 pages, 382 KiB

Open AccessEditorial

Phenotypic and Functional Diversity of Mast Cells

by Satoshi Tanaka

Int. J. Mol. Sci. 2020, 21(11), 3835; https://doi.org/10.3390/ijms21113835 - 28 May 2020

Cited by 6 | Viewed by 1781

Abstract

Mast cells, which originate from hematopoietic stem cells, are distributed in nearly all vascularized tissues [...] Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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Research

Jump to: Editorial, Review

11 pages, 6207 KiB

Open AccessArticle

Identification of 5-Hydroxymethylfurfural (5-HMF) as an Active Component Citrus Jabara That Suppresses FcεRI-Mediated Mast Cell Activation

by Ryota Uchida, Michiko Kato, Yuka Hattori, Hiroko Kikuchi, Emi Watanabe, Katsuumi Kobayashi and Keigo Nishida

Int. J. Mol. Sci. 2020, 21(7), 2472; https://doi.org/10.3390/ijms21072472 - 02 Apr 2020

Cited by 12 | Viewed by 2893

Abstract

Jabara (Citrus jabara Hort. ex Y. Tanaka) is a type of citrus fruit known for its beneficial effect against seasonal allergies. Jabara is rich in the antioxidant narirutin whose anti-allergy effect has been demonstrated. One of the disadvantages in consuming Jabara is its bitter flavor. Therefore, we fermented the fruit to reduce the bitterness and make Jabara easy to consume. Here, we examined whether fermentation alters the anti-allergic property of Jabara. Suppression of degranulation and cytokine production was observed in mast cells treated with fermented Jabara and the effect was dependent on the length of fermentation. We also showed that 5-hydroxymethylfurfural (5-HMF) increases as fermentation progresses and was identified as an active component of fermented Jabara, which inhibited mast cell degranulation. Mast cells treated with 5-HMF also exhibited reduced degranulation and cytokine production. In addition, we showed that the expression levels of phospho-PLCγ1 and phospho-ERK1/2 were markedly reduced upon FcεRI stimulation. These results indicate that 5-HMF is one of the active components of fermented Jabara that is involved in the inhibition of mast cell activation. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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13 pages, 4900 KiB

Open AccessCommunication

Clinical Significance of Cytoplasmic IgE-Positive Mast Cells in Eosinophilic Chronic Rhinosinusitis

by Yuka Gion, Mitsuhiro Okano, Takahisa Koyama, Tokie Oura, Asami Nishikori, Yorihisa Orita, Tomoyasu Tachibana, Hidenori Marunaka, Takuma Makino, Kazunori Nishizaki and Yasuharu Sato

Int. J. Mol. Sci. 2020, 21(5), 1843; https://doi.org/10.3390/ijms21051843 - 07 Mar 2020

Cited by 9 | Viewed by 2743

Abstract

Cross-linking of antigen-specific IgE bound to the high-affinity IgE receptor (FcεRI) on the surface of mast cells with multivalent antigens results in the release of mediators and development of type 2 inflammation. FcεRI expression and IgE synthesis are, therefore, critical for type 2 inflammatory disease development. In an attempt to clarify the relationship between eosinophilic chronic rhinosinusitis (ECRS) and mast cell infiltration, we analyzed mast cell infiltration at lesion sites and determined its clinical significance. Mast cells are positive for c-kit, and IgE in uncinated tissues (UT) and nasal polyps (NP) were examined by immunohistochemistry. The number of positive cells and clinicopathological factors were analyzed. Patients with ECRS exhibited high levels of total IgE serum levels and elevated peripheral blood eosinophil ratios. As a result, the number of mast cells with membranes positive for c-kit and IgE increased significantly in lesions forming NP. Therefore, we classified IgE-positive mast cells into two groups: membrane IgE-positive cells and cytoplasmic IgE-positive cells. The amount of membrane IgE-positive mast cells was significantly increased in moderate ECRS. A positive correlation was found between the membrane IgE-positive cells and the radiological severity score, the ratio of eosinophils, and the total serum IgE level. The number of cytoplasmic IgE-positive mast cells was significantly increased in moderate and severe ECRS. A positive correlation was observed between the cytoplasmic IgE-positive cells and the radiological severity score, the ratio of eosinophils in the blood, and the total IgE level. These results suggest that the process of mast cell internalization of antigens via the IgE receptor is involved in ECRS pathogenesis. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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13 pages, 1366 KiB

Open AccessArticle

Establishment and Characterization of a Murine Mucosal Mast Cell Culture Model

by Aya Kakinoki, Tsuyoshi Kameo, Shoko Yamashita, Kazuyuki Furuta and Satoshi Tanaka

Int. J. Mol. Sci. 2020, 21(1), 236; https://doi.org/10.3390/ijms21010236 - 29 Dec 2019

Cited by 7 | Viewed by 3212

Abstract

Accumulating evidence suggests that mast cells play critical roles in disruption and maintenance of intestinal homeostasis, although it remains unknown how they affect the local microenvironment. Interleukin-9 (IL-9) was found to play critical roles in intestinal mast cell accumulation induced in various pathological conditions, such as parasite infection and oral allergen-induced anaphylaxis. Newly recruited intestinal mast cells trigger inflammatory responses and damage epithelial integrity through release of a wide variety of mediators including mast cell proteases. We established a novel culture model (IL-9-modified mast cells, MCs/IL-9), in which murine IL-3-dependent bone-marrow-derived cultured mast cells (BMMCs) were further cultured in the presence of stem cell factor and IL-9. In MCs/IL-9, drastic upregulation of Mcpt1 and Mcpt2 was found. Although histamine storage and tryptase activity were significantly downregulated in the presence of SCF and IL-9, this was entirely reversed when mast cells were cocultured with a murine fibroblastic cell line, Swiss 3T3. MCs/IL-9 underwent degranulation upon IgE-mediated antigen stimulation, which was found to less sensitive to lower concentrations of IgE in comparison with BMMCs. This model might be useful for investigation of the spatiotemporal changes of newly recruited intestinal mast cells. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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12 pages, 1700 KiB

Open AccessArticle

The Putatively Specific Synthetic REV-ERB Agonist SR9009 Inhibits IgE- and IL-33-Mediated Mast Cell Activation Independently of the Circadian Clock

by Kayoko Ishimaru, Shotaro Nakajima, Guannan Yu, Yuki Nakamura and Atsuhito Nakao

Int. J. Mol. Sci. 2019, 20(24), 6320; https://doi.org/10.3390/ijms20246320 - 14 Dec 2019

Cited by 9 | Viewed by 4145

Abstract

The cell-autonomous circadian clock regulates IgE- and IL-33-mediated mast cell activation, both of which are key events in the development of allergic diseases. Accordingly, clock modifiers could be used to treat allergic diseases, as well as many other circadian-related diseases, such as sleep and metabolic disorders. The nuclear receptors REV-ERB-α and -β (REV-ERBs) are crucial components of the circadian clockwork. Efforts to pharmacologically target REV-ERBs using putatively specific synthetic agonists, particularly SR9009, have yielded beneficial effects on sleep and metabolism. Here, we sought to determine whether REV-ERBs are functional in the circadian clockwork in mast cells and, if so, whether SR9009 affects IgE- and IL-33-mediated mast cell activation. Bone marrow-derived mast cells (BMMCs) obtained from wild-type mice expressed REV-ERBs, and SR9009 or other synthetic REV-ERBs agonists affected the mast cell clockwork. SR9009 inhibited IgE- and IL-33-mediated mast cell activation in wild-type BMMCs in association with inhibition of Gab2/PI3K and NF-κB activation. Unexpectedly, these suppressive effects of SR9009 were observed in BMMCs following mutation of the core circadian gene Clock. These findings suggest that SR9009 inhibits IgE- and IL-33-mediated mast cell activation independently of the functional circadian clock activity. Thus, SR9009 or other synthetic REV-ERB agonists may have potential for anti-allergic agents. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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17 pages, 13793 KiB

Open AccessArticle

Repeated Vaginal Exposures to the Common Cosmetic and Household Preservative Methylisothiazolinone Induce Persistent, Mast Cell-Dependent Genital Pain in ND4 Mice

by Erica Arriaga-Gomez, Jaclyn Kline, Elizabeth Emanuel, Nefeli Neamonitaki, Tenzin Yangdon, Hayley Zacheis, Dogukan Pasha, Jinyoung Lim, Susan Bush, Beebie Boo, Hanna Mengistu, Ruby Kinnamon, Robin Shields-Cutler, Elizabeth Wattenberg and Devavani Chatterjea

Int. J. Mol. Sci. 2019, 20(21), 5361; https://doi.org/10.3390/ijms20215361 - 28 Oct 2019

Cited by 11 | Viewed by 7195

Abstract

A history of allergies doubles the risk of vulvodynia—a chronic pain condition of unknown etiology often accompanied by increases in numbers of vulvar mast cells. We previously established the biological plausibility of this relationship in mouse models where repeated exposures to the allergens oxazolone or dinitrofluorobenzene on the labiar skin or inside the vaginal canal of ND4 Swiss Webster outbred mice led to persistent tactile sensitivity and local increases in mast cells. In these models, depletion of mast cells alleviated pain. While exposure to cleaning chemicals has been connected to elevated vulvodynia risk, no single agent has been linked to adverse outcomes. We sensitized female mice to methylisothiazolinone (MI)—a biocide preservative ubiquitous in cosmetics and cleaners—dissolved in saline on their flanks, and subsequently challenged them with MI or saline for ten consecutive days in the vaginal canal. MI-challenged mice developed persistent tactile sensitivity, increased vaginal mast cells and eosinophils, and had higher serum Immunoglobulin E. Therapeutic and preventive intra-vaginal administration of Δ⁹-tetrahydrocannabinol reduced mast cell accumulation and tactile sensitivity. MI is known to cause skin and airway irritation in humans, and here we provide the first pre-clinical evidence that repeated MI exposures can also provoke allergy-driven genital pain. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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16 pages, 2303 KiB

Open AccessArticle

Identification of Gain and Loss of Function Missense Variants in MRGPRX2’s Transmembrane and Intracellular Domains for Mast Cell Activation by Substance P

by Chalatip Chompunud Na Ayudhya, Saptarshi Roy, Ibrahim Alkanfari, Anirban Ganguly and Hydar Ali

Int. J. Mol. Sci. 2019, 20(21), 5247; https://doi.org/10.3390/ijms20215247 - 23 Oct 2019

Cited by 48 | Viewed by 4317

Abstract

The neuropeptide substance P (SP) contributes to neurogenic inflammation through the activation of human mast cells via Mas-related G protein-coupled receptor-X2 (MRGPRX2). Using pertussis toxins and YM-254890, we demonstrated that SP induces Ca²⁺ mobilization and degranulation via both the Gαi and Gαq family of G proteins in rat basophilic leukemia (RBL-2H3) cells stably expressing MRGPRX2. To determine the roles of MRGPRX2’s transmembrane (TM) and intracellular domains on SP-induced responses, we utilized information obtained from both structural modeling and naturally occurring MRGPRX2 missense variants. We found that highly conserved residues in TM6 (I225) and TM7 (Y279) of MRGPRX2 are essential for SP-induced Ca²⁺ mobilization and degranulation in transiently transfected RBL-2H3 cells. Cells expressing missense variants in the receptor’s conserved residues (V123F and V282M) as well as intracellular loops (R138C and R141C) failed to respond to SP. By contrast, replacement of all five Ser/Thr residues with Ala and missense variants (S325L and L329Q) in MRGPRX2’s carboxyl-terminus resulted in enhanced mast cell activation by SP when compared to the wild-type receptor. These findings suggest that MRGPRX2 utilizes conserved residues in its TM domains and intracellular loops for coupling to G proteins and likely undergoes desensitization via phosphorylation at Ser/Thr residues in its carboxyl-terminus. Furthermore, identification of gain and loss of function MRGPRX2 variants has important clinical implications for SP-mediated neurogenic inflammation and other chronic inflammatory diseases. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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15 pages, 4027 KiB

Open AccessArticle

Co-Stimulation of Purinergic P2X4 and Prostanoid EP3 Receptors Triggers Synergistic Degranulation in Murine Mast Cells

by Kazuki Yoshida, Makoto Tajima, Tomoki Nagano, Kosuke Obayashi, Masaaki Ito, Kimiko Yamamoto and Isao Matsuoka

Int. J. Mol. Sci. 2019, 20(20), 5157; https://doi.org/10.3390/ijms20205157 - 17 Oct 2019

Cited by 15 | Viewed by 2860

Abstract

Mast cells (MCs) recognize antigens (Ag) via IgE-bound high affinity IgE receptors (FcεRI) and trigger type I allergic reactions. FcεRI-mediated MC activation is regulated by various G protein-coupled receptor (GPCR) agonists. We recently reported that ionotropic P2X4 receptor (P2X4R) stimulation enhanced FcεRI-mediated degranulation. Since MCs are involved in Ag-independent hypersensitivity, we investigated whether co-stimulation with ATP and GPCR agonists in the absence of Ag affects MC degranulation. Prostaglandin E₂ (PGE₂) induced synergistic degranulation when bone marrow-derived MCs (BMMCs) were co-stimulated with ATP, while pharmacological analyses revealed that the effects of PGE₂ and ATP were mediated by EP3 and P2X4R, respectively. Consistently, this response was absent in BMMCs prepared from P2X4R-deficient mice. The effects of ATP and PGE₂ were reduced by PI3 kinase inhibitors but were insensitive to tyrosine kinase inhibitors which suppressed the enhanced degranulation induced by Ag and ATP. MC-dependent PGE₂-triggered vascular hyperpermeability was abrogated in a P2X4R-deficient mouse ear edema model. Collectively, our results suggest that P2X4R signaling enhances EP3R-mediated MC activation via a different mechanism to that involved in enhancing Ag-induced responses. Moreover, the cooperative effects of the common inflammatory mediators ATP and PGE₂ on MCs may be involved in Ag-independent hypersensitivity in vivo. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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18 pages, 5385 KiB

Open AccessArticle

Highly Selective Cleavage of TH2-Promoting Cytokines by the Human and the Mouse Mast Cell Tryptases, Indicating a Potent Negative Feedback Loop on TH2 Immunity

by Zhirong Fu, Srinivas Akula, Michael Thorpe and Lars Hellman

Int. J. Mol. Sci. 2019, 20(20), 5147; https://doi.org/10.3390/ijms20205147 - 17 Oct 2019

Cited by 27 | Viewed by 4297

Abstract

Mast cells (MC) are resident tissue cells found primarily at the interphase between tissues and the environment. These evolutionary old cells store large amounts of proteases within cytoplasmic granules, and one of the most abundant of these proteases is tryptase. To look deeper into the question of their in vivo targets, we have analyzed the activity of the human MC tryptase on 69 different human cytokines and chemokines, and the activity of the mouse tryptase (mMCP-6) on 56 mouse cytokines and chemokines. These enzymes were found to be remarkably restrictive in their cleavage of these potential targets. Only five were efficiently cleaved by the human tryptase: TSLP, IL-21, MCP3, MIP-3b, and eotaxin. This strict specificity indicates a regulatory function of these proteases and not primarily as unspecific degrading enzymes. We recently showed that the human MC chymase also had a relatively strict specificity, indicating that both of these proteases have regulatory functions. One of the most interesting regulatory functions may involve controlling excessive TH2-mediated inflammation by cleaving several of the most important TH2-promoting inflammatory cytokines, including IL-18, IL-33, TSLP, IL-15, and IL-21, indicating a potent negative feedback loop on TH2 immunity. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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17 pages, 2482 KiB

Open AccessArticle

Mouse Tryptase Gene Expression is Coordinately Regulated by GATA1 and GATA2 in Bone Marrow-Derived Mast Cells

by Kinuko Ohneda, Shin’ya Ohmori and Masayuki Yamamoto

Int. J. Mol. Sci. 2019, 20(18), 4603; https://doi.org/10.3390/ijms20184603 - 17 Sep 2019

Cited by 14 | Viewed by 3883

Abstract

Mast cell tryptases have crucial roles in allergic and inflammatory diseases. The mouse tryptase genes represent a cluster of loci on chromosome 16p3.3. While their functional studies have been extensively performed, transcriptional regulation of tryptase genes is poorly understood. In this study, we examined the molecular basis of the tryptase gene expression in bone marrow-derived mast cells (BMMCs) of C57BL/6 mice and in MEDMC-BRC6 mast cells. The expression of the Tpsb2 and Tpsg1 genes, which reside at the 3′-end of the tryptase locus, is significantly decreased by the reduction of the GATA transcription factors GATA1 or GATA2. Chromatin immunoprecipitation assays have shown that the GATA factors bind at multiple regions within the locus, including 1.0 and 72.8 kb upstream of the Tpsb2 gene, and that GATA1 and GATA2 facilitate each other’s DNA binding activity to these regions. Deletion of the −72.8 kb region by genome editing significantly reduced the Tpsb2 and Tpsg1 mRNA levels in MEDMC-BRC6 cells. Furthermore, binding of CTCF and the cohesin subunit Rad21 was found upstream of the −72.8 kb region and was significantly reduced in the absence of GATA1. These results suggest that mouse tryptase gene expression is coordinately regulated by GATA1 and GATA2 in BMMCs. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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Review

Jump to: Editorial, Research

16 pages, 858 KiB

Open AccessReview

Beyond IgE: Alternative Mast Cell Activation Across Different Disease States

by David O. Lyons and Nicholas A. Pullen

Int. J. Mol. Sci. 2020, 21(4), 1498; https://doi.org/10.3390/ijms21041498 - 22 Feb 2020

Cited by 50 | Viewed by 11448

Abstract

Mast cells are often regarded through the lens of IgE-dependent reactions as a cell specialized only for anti-parasitic and type I hypersensitive responses. However, recently many researchers have begun to appreciate the expansive repertoire of stimuli that mast cells can respond to. After the characterization of the interleukin (IL)-33/suppression of tumorigenicity 2 (ST2) axis of mast cell activation—a pathway that is independent of the adaptive immune system—researchers are revisiting other stimuli to induce mast cell activation and/or subsequent degranulation independent of IgE. This discovery also underscores that mast cells act as important mediators in maintaining body wide homeostasis, especially through barrier defense, and can thus be the source of disease as well. Particularly in the gut, inflammatory bowel diseases (Crohn’s disease, ulcerative colitis, etc.) are characterized with enhanced mast cell activity in the context of autoimmune disease. Mast cells show phenotypic differences based on tissue residency, which could manifest as different receptor expression profiles, allowing for unique mast cell responses (both IgE and non-IgE mediated) across varying tissues as well. This variety in receptor expression suggests mast cells respond differently, such as in the gut where immunosuppressive IL-10 stimulates the development of food allergy or in the lungs where transforming growth factor-β1 (TGF-β1) can enhance mast cell IL-6 production. Such differences in receptor expression illustrate the truly diverse effector capabilities of mast cells, and careful consideration must be given toward the phenotype of mast cells observed in vitro. Given mast cells’ ubiquitous tissue presence and their capability to respond to a broad spectrum of non-IgE stimuli, it is expected that mast cells may also contribute to the progression of autoimmune disorders and other disease states such as metastatic cancer through promoting chronic inflammation in the local tissue microenvironment and ultimately polarizing toward a unique T_h17 immune response. Furthermore, these interconnected, atypical activation pathways may crosstalk with IgE-mediated signaling differently across disorders such as parasitism, food allergies, and autoimmune disorders of the gut. In this review, we summarize recent research into familiar and novel pathways of mast cells activation and draw connections to clinical human disease. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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15 pages, 720 KiB

Open AccessReview

Killer Immunoglobulin-Like Receptor 2DL4 (CD158d) Regulates Human Mast Cells both Positively and Negatively: Possible Roles in Pregnancy and Cancer Metastasis

by Tatsuki R. Kataoka, Chiyuki Ueshima, Masahiro Hirata, Sachiko Minamiguchi and Hironori Haga

Int. J. Mol. Sci. 2020, 21(3), 954; https://doi.org/10.3390/ijms21030954 - 31 Jan 2020

Cited by 15 | Viewed by 3772

Abstract

Killer immunoglobulin-like receptor (KIR) 2DL4 (CD158d) was previously thought to be a human NK cell-specific protein. Mast cells are involved in allergic reactions via their KIT-mediated and FcɛRI-mediated responses. We recently detected the expression of KIR2DL4 in human cultured mast cells established from peripheral blood of healthy volunteers (PB-mast), in the human mast cell line LAD2, and in human tissue mast cells. Agonistic antibodies against KIR2DL4 negatively regulate the KIT-mediated and FcɛRI-mediated responses of PB-mast and LAD2 cells. In addition, agonistic antibodies and human leukocyte antigen (HLA)-G, a natural ligand for KIR2DL4, induce the secretion of leukemia inhibitory factor and serine proteases from human mast cells, which have been implicated in pregnancy establishment and cancer metastasis. Therefore, KIR2DL4 stimulation with agonistic antibodies and recombinant HLA-G protein may enhance both processes, in addition to suppressing mast-cell-mediated allergic reactions. Full article

(This article belongs to the Special Issue Activation and Modulation of Mast Cells)

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