Development, significance, and heterogeneity of mast cells with particular regard to the mast cell-specific proteases chymase and tryptase

Welle, Monika Maria

doi:10.1002/jlb.61.3.233

Cited by 317 publications

(296 citation statements)

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“…Humans express only one mast cell chymase, whereas mature murine mast cells express mMCP-1, mMCP-2, mMCP-4, and/or mMCP-5, depending on tissue location, substrate specificity, and affinity for proteoglycans. Mast cell expression of neutral proteases typically ascribed to the mucosal mast cell subset (mMCP-1 and mMCP-2) or the CTMC subset (mMCP-4, mMCP-5, mMCP-6, and carboxypeptidase) was examined (49). We reported previously that mast cells in the murine conjunctiva are CTMCs (55), a finding that was confirmed in this study by immunostaining for mMCP-4.…”

Section: Discussionsupporting

confidence: 78%

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Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Kuo

Collins

Boettner

et al. 2017

The Journal of Immunology

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Molecules that are necessary for ocular hypersensitivity reactions include the receptors CCR1 and CCR3; CCL7 is a ligand for these receptors. Therefore, we explored the role of CCL7 in mast cell activity and motility in vitro and investigated the requirement for CCL7 in a murine model of IgE-mediated allergic conjunctivitis. For mast cells treated with IgE and Ag, the presence of CCL7 synergistically enhanced degranulation and calcium influx. CCL7 also induced chemotaxis in mast cells. CCL7-deficient bone marrow–derived mast cells showed decreased degranulation following IgE and Ag treatment compared with wild-type bone marrow–derived mast cells, but there was no difference in degranulation when cells were activated via an IgE-independent pathway. In vivo, CCL7 was upregulated in conjunctival tissue during an OVA-induced allergic response. Notably, the early-phase clinical symptoms in the conjunctiva after OVA challenge were significantly higher in OVA-sensitized wild-type mice than in control challenged wild-type mice; the increase was suppressed in CCL7-deficient mice. In the OVA-induced allergic response, the numbers of conjunctival mast cells were lower in CCL7-deficient mice than in wild-type mice. Our results demonstrate that CCL7 is required for maximal OVA-induced ocular anaphylaxis, mast cell recruitment in vivo, and maximal FcεRI-mediated mast cell activation in vitro. A better understanding of the role of CCL7 in mediating ocular hypersensitivity reactions will provide insights into mast cell function and novel treatments for allergic ocular diseases.

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Section: Discussionsupporting

confidence: 78%

“…*p , 0.05, **p , 0.01, ANOVA. (49). To further characterize local mast cells in the allergic conjunctiva, we performed immunofluorescence staining to identify mMCP-4-containing mast cells.…”

Section: Ccl7 2/2 Mice Display Markedly Reduced Clinical Symptoms Of mentioning

confidence: 99%

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Kuo

Collins

Boettner

et al. 2017

The Journal of Immunology

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“…Moreover, tryptase causes eosinophil degranulation (7) and contraction of bronchial smooth muscle (45). Tryptase inhibitors suppress not only the early phase but also the late phase of allergic inflammation, indicating tryptase influences on infiltrated inflammatory cells and on cytokine/chemokine production (46,47).…”

Section: Discussionmentioning

confidence: 99%

Tryptase Activates the Mitogen-Activated Protein Kinase/Activator Protein-1 Pathway in Human Peripheral Blood Eosinophils, Causing Cytokine Production and Release

Temkin¹,

Kantor²,

Weg³

et al. 2002

The Journal of Immunology

114

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We have previously shown that mast cells enhance eosinophil survival and activation. In this study we further characterized mast cell activity toward eosinophils. Sonicate of both rat peritoneal mast cells and the human mast cell line 1 (HMC-1) induced a concentration-dependent IL-6 and IL-8 release from human peripheral blood eosinophils (ELISA). HMC-1-induced IL-8 release was significantly reduced by the tryptase inhibitors GW-45 and GW-58 (90 and 87%, respectively, at an optimal concentration) but not by anti-stem cell factor, anti-TNF-α, or anti-IFN-γ neutralizing Abs or by the antihistamine drugs pyrilamine and cimetidine. In a manner similar to HMC-1, human recombinant tryptase induced the expression of mRNA for IL-8 (RT-PCR) and caused IL-8 release from the eosinophils. Addition of cycloheximide, actinomycin D, dexamethasone, PD 98059, curcumin, or SB 202190 completely inhibited the tryptase-induced IL-6 and IL-8 release. In contrast, cyclosporin A had no effect on tryptase-induced IL-8 release. Tryptase caused phosphorylation of extracellular signal-regulated kinases 1 and 2, c-Jun N-terminal kinases 1 and 2, and p38 (Western blot). Tryptase also induced the translocation of c-Jun from the cytosol to the nucleus (confocal microscopy) and enhanced AP-1 binding activity to the DNA (EMSA). Eosinophils were found to express proteinase-activated receptor 2 (FACS). When eosinophils were incubated with tryptase in the presence of anti-proteinase-activated receptor 2 antagonist Abs a significant decrease in the IL-6 and IL-8 release occurred. In summary, we have demonstrated that the preformed mast cell mediator tryptase induces cytokine production and release in human peripheral blood eosinophils by the mitogen-activated protein kinase/AP-1 pathway.

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“…These cells produce an array of vasoactive mediators and proinflammatory substances, like cytokines, histamine, protease, leukotrienes, tumor necrosis factor-α (TNF-α) and others (Welle, 1997;Shichijo et al, 1999;Brazis et al, 2000;Malaviya and Abraham, 2000;Yamashita et al, 2000). Among the preformed and newly synthesized inflammatory substances released upon degranulation of mast cells, histamine is the best characterized and most potent vasoactive mediator implicated in the anaphylaxis (Petersen et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

Atrial natriuretic peptide induces rat peritoneal mast cell activation by cGMP-independent and calcium uptake-dependent mechanism

Chai

Lee²,

Han³

et al. 2000

Exp Mol Med

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Atrial natriuretic peptide (ANP), a 28 amino acid basic polypeptide, is known to induce histamine release from human and rat mast cells in vitro and cause a wheel formation in rat skin. However, cellular events associated with histamine release are not clearly understood. In this study, we have examined the calcium flux and cGMP formation associated with histamine release in the ANP-treated mast cells. ANP, in vitro, induced mast cell degranulation and histamine release in a dose-dependent manner. ANP also induced an enhanced calcium uptake into cells and increased the cellular level of cGMP in mast cells. A high level of calcium in the media caused an inhibition of ANP-dependent histamine release but enhanced the level of intracellular cGMP of mast cells. ANP inducing a dose-dependent increase in vascular permeability of rat skin was confirmed by the extravasation of the circulating Evans blue. The results indicate ANP induced the histamine release and an increase in vascular permeability through mast cell degranulation in cGMP-independent and calcium uptake-dependent manner.

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Development, significance, and heterogeneity of mast cells with particular regard to the mast cell-specific proteases chymase and tryptase

Abstract: Abstract:Mast

Cited by 317 publications

References 0 publications

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Tryptase Activates the Mitogen-Activated Protein Kinase/Activator Protein-1 Pathway in Human Peripheral Blood Eosinophils, Causing Cytokine Production and Release

Atrial natriuretic peptide induces rat peritoneal mast cell activation by cGMP-independent and calcium uptake-dependent mechanism

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