Human synovial mast cells. I. Ultrastructural in situ and in vitro immunologic characterization

Paulis, Amato de; Marinò, Isabella; Ciccarelli, Andrea; Crescenzo, Gennaro de; Concardi, Monica; Verga, Laura; Arbustini, Eloisa; Marone, Gianni

doi:10.1002/art.1780390723

Cited by 76 publications

(90 citation statements)

References 49 publications

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“…32 PGMD contains 0.25 g/L MgCl 2 ⅐ 6H 2 O, 10 mg/L DNase, and 1 g/L gelatin in addition to P, pH 7.37.…”

Section: Buffersmentioning

confidence: 99%

“…Tryptase, a neutral protease stored in the cytoplasmic granules of all human mast cells, 24,32,38 can be released from human mast cells 24,31 and is a potent mitogen for human fibroblasts. 39 The tryptase content of heart tissue from patients with DCM (32.3Ϯ5.9 g/g wet tissue) and ICM (33.7Ϯ4.3 g/g wet tissue) was higher than that of control subjects (6.9Ϯ2.1 g/g wet tissue) (PϽ.05).…”

Section: Tryptase Content In the Failing Heartmentioning

confidence: 99%

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Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

et al. 1998

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Background-We compared cardiac mast cell (HHMC) density and the immunological and nonimmunological release of mediators from mast cells isolated from heart tissue of patients with idiopathic dilated (DCM) (nϭ24) and ischemic cardiomyopathy (ICM) (nϭ10) undergoing heart transplantation and from control subjects (nϭ10) without cardiovascular disease. Methods and Results-HHMC density in DCM (18.4Ϯ1.6 cells/mm 2 ) and ICM (18.4Ϯ1.5 cells/mm 2 ) was higher than that in control hearts (5.3Ϯ0.7 cells/mm 2 ; PϽ.01). The histamine and tryptase contents of DCM and ICM hearts were higher than those of control hearts. The histamine content of the hearts was correlated with mast cell density (r s ϭ.91; PϽ.001). Protein A/gold staining of heart tissue revealed stem cell factor (SCF), the principal growth, differentiating, and activating factor of human mast cells, in HHMC secretory granules. Histamine release from cardiac mast cells caused by immunological (anti-IgE and rhSCF) and nonimmunological stimuli (Ca 2ϩ ionophore A23187) was higher in patients with DCM and ICM compared with control subjects. Immunological activation of HHMC induced a significantly greater release of tryptase and LTC 4 in patients with DCM and ICM compared with control subjects. Conclusions-Histamine and tryptase content and mast cell density are higher in failing hearts than in control hearts. SCF, present in secretory granules of HHMC, might represent an autocrine factor sustaining mast cell hyperplasia in heart tissue in these patients. The increased local release of fibrogenic factors (eg, histamine, tryptase, and leukotriene C 4 ) might contribute to collagen accumulation in the hearts of patients with cardiomyopathy. 1 Mast cells are present in human heart tissue 2,3 and in adventia and intima of coronary arteries of patients with coronary artery disease. [4][5][6] Moreover, the in vitro immunological activation of human heart tissue with anti-IgE induces the release of histamine and prostaglandin D 2 . 7,8 The concentration of histamine and the density of mast cells are increased in the arteries of cardiac patients, 4,5,9 and coronary arteries from cardiac patients are hyperresponsive in vitro to histamine. 4 Furthermore, in vivo administration of histamine and other mast cell-derived mediators (peptide LTC 4 ) in humans causes significant cardiovascular effects. 10 -12 Finally, serum IgE levels are increased in patients with coronary artery disease. 13,14 Taken together, these observations raise the possibility that local activation of cardiac mast cells might contribute, through the release of vasoactive mediators, to certain cardiovascular diseases. 15,16 Fibrosis is a hallmark of failing hearts in DCM and ICM. 17 The cells and the mediators responsible for fibroblast proliferation and collagen accumulation in failing hearts in DCM and ICM are largely unknown. Mast cells are involved in many types of inflammation and repair processes and are found in increased numbers in fibrotic tissues. For example, increased mast cell density has be...

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“…32 PGMD contains 0.25 g/L MgCl 2 ⅐ 6H 2 O, 10 mg/L DNase, and 1 g/L gelatin in addition to P, pH 7.37.…”

Section: Buffersmentioning

confidence: 99%

Section: Tryptase Content In the Failing Heartmentioning

confidence: 99%

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

et al. 1998

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“…Resected joint tissue was immediately immersed in cold (4°C) PIPES buffer and processed within 2 hours of removal, using a recently described technique (9). Fat, cartilage, and fibrous tissue were removed.…”

Section: Methodsmentioning

confidence: 99%

“…Recent studies have extensively characterized in situ and in vitro some of the immunologic and biochemical features of HSyMC (4,9). However, except for two studies (6,7), the pharmacologic modulation of HSyMC is largely unexplored.…”

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confidence: 99%

Human synovial mast cells. II. Heterogeneity of the pharmacologic effects of antiinflammatory and immunosuppressive drugs

Paulis

Ciccarelli

Marinò

et al. 1997

Arthritis & Rheumatism

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Objective. To evaluate the in vitro effects of 4 antiinflammatory and 5 immunosuppressive agents on the release of preformed and de novo‐synthesized mediators from human synovial mast cells (HSyMC) activated by immunologic and nonimmunologic stimuli. Methods. The effects of antiinflammatory and immunosuppressive agents were evaluated on the in vitro release of histamine and tryptase and the de novo synthesis of prostaglandin D2 (PGD2) and leukotriene C4 (LTC4) by HSyMC challenged with anti‐IgE and substance P. Results. Nimesulide, a sulfonanilide nonsteroidal antiinflammatory drug (NSAID) chemically unrelated to other acidic NSAIDs (such as acetylsalicylic acid [ASA], diclofenac, and piroxicam) inhibited in a concentration‐dependent manner the release of preformed (histamine and tryptase) mediators from HSyMC challenged with anti‐IgE. In contrast, diclofenac and piroxicam had little or no effect on HSyMC activated by anti‐IgE. ASA, diclofenac, piroxicam, and nimesulide caused a concentration‐dependent inhibition of IgE‐mediated PGD2 release from HSyMC. Nimesulide, but not diclofenac or piroxicam, also inhibited the de novo synthesis of LTC4 by HSyMC challenged with anti‐IgE. Nimesulide, diclofenac, and piroxicam had no effect on HSyMC activated by substance P. Cyclosporin A (CSA) inhibited histamine release from HSyMC challenged with anti‐IgE, whereas cyclosporin H (CSH) had no effect. FK‐506 also inhibited histamine release from HSyMC activated by anti‐IgE, whereas rapamycin had no effect. Neither CSA, CSH, FK‐506, nor rapamycin inhibited the release of histamine from HSyMC induced by substance P. Methotrexate had no effect on the release of mediators from these cells, whereas adenosine (R‐phenylisopropyl adenosine and 5‐N‐ethylcarboxamide adenosine) enhanced histamine release from immunologically activated HSyMC in a concentration‐dependent manner. Conclusion. Mast cells isolated from human synovia display 4 levels of pharmacologic heterogeneity with regard to 1) the inhibitory effects of 4 antiinflammatory drugs; 2) the capacity of different immunosuppressive drugs to exert antiinflammatory activity; 3) the inhibition of the release of different mediators; and 4) the capacity of antiinflammatory and immunosuppressive drugs to modulate HSyMC activated by different stimuli. This complexity of pharmacologic modulation of HSyMC in vitro might help explain the different activity of the compounds used to treat various pathophysiologic aspects of the inflammatory arthritides.

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“…Human tryptase is a tetrameric serine protease that is concentrated and stored selectively in the secretory granules of human mast cells; during mast cell activation, it is secreted into the circulation (2). Given that tryptase is expressed in the synovial tissue of patients with RA (3), we tested whether tryptase levels are also elevated in the sera of RA patients and investigated for a possible correlation with markers of disease activity.…”

Section: To the Editormentioning

confidence: 99%

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Rivellese

Paulis

Marone

et al. 2016

Arthritis & Rheumatology

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Human synovial mast cells. I. Ultrastructural in situ and in vitro immunologic characterization

Cited by 76 publications

References 49 publications

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

Human synovial mast cells. II. Heterogeneity of the pharmacologic effects of antiinflammatory and immunosuppressive drugs

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