The activation of synovial mast cells: modulation of histamine release by tryptase and chymase and their inhibitors

He, Shaoheng; Gaça, Marianna; Walls, Andrew F.

doi:10.1016/s0014-2999(01)00734-8

Cited by 101 publications

(113 citation statements)

References 28 publications

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“…Thus, there are at least two self-amplification mechanisms in human mast cells upon degranulation, including tryptase and PAR-2 feedback process previously reported [22,23] and histamine inducing tryptase release.…”

Section: Discussionmentioning

confidence: 89%

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Modulation of tryptase secretion from human colon mast cells by histamine

Xie²

2004

WJG

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AIM:To investigate the ability of histamine to modulate tryptase release from human colon mast cells and the potential mechanisms. METHODS:Enzymatically dispersed cells from human colons were challenged with histamine, anti-IgE or calcium ionophore A23187 (CI), and the cell supernatants after challenge were collected. Tryptase release was determined with a sandwich ELISA procedure. RESULTS:Histamine at concentrations from 1 ng/mL was able to induce a "bell" shape dose related release of tryptase from colon mast cells. The maximum release of tryptase was approximately 3.5 fold more than spontaneous release. As little as 10 ng/mL histamine showed a similar potency to 10 µg/mL anti-IgE in induction of tryptase release. Histamine induced release of tryptase initiated at 10 s when histamine (100 ng/mL) was added to cells, gradually increased thereafter, and completed at 5 min. Both pertussis toxin or metabolic inhibitors were able to inhibit histamine induced tryptase release. When histamine and anti-IgE were added to colon mast cells at the same time, the quantity of tryptase released was similar to that induced by anti-IgE alone. The similar results were observed with CI. However, when various concentrations of histamine were incubated with cells for 20 min before adding anti-IgE or CI, the quantity of tryptase released was similar to that was induced by histamine alone. CONCLUSION:Histamine is a potent activator of human colon mast cells, which represents a novel and pivotal selfamplification mechanism of mast cell degranulation.

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Section: Discussionmentioning

confidence: 89%

“…The mast cell dispersion procedure was similar to that described 324 ISSN 1007-9327 CN 14-1219/ R World J Gastroenterol February 1, 2004 Volume 10 Number 3 previously [21,22] . Human colon tissue was obtained from patients with carcinoma of colon at colectomy.…”

Section: Dispersion Of Mast Cellsmentioning

confidence: 99%

Modulation of tryptase secretion from human colon mast cells by histamine

Xie²

2004

WJG

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“…There is considerable circumstantial evidence implicating mast cells in the pathogenesis of human rheumatoid arthritis (RA). These include the production of inflammatory (13,14) and tissue destructive (15,16) mediators. Moreover, a significant increase in mast cell numbers has been documented in human synovial tissue derived from patients with RA (8,9).…”

Section: Ast Cells Are Derived From Hemopoietic Progenitor Cells Thmentioning

confidence: 99%

Human Mast Cell-Derived Gelatinase B (Matrix Metalloproteinase-9) Is Regulated by Inflammatory Cytokines: Role in Cell Migration

Girolamo

Indoh

Jackson

et al. 2006

The Journal of Immunology

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Mast cells are key effectors in the pathogenesis of inflammatory and tissue destructive diseases such as rheumatoid arthritis (RA). These cells contain specialized secretory granules loaded with bioactive molecules including cytokines, growth factors, and proteases that are released upon activation. This study investigated the regulation of matrix metalloproteinase MMP-9 (gelatinase B) in human mast cells by cytokines that are known to be involved in the pathogenesis of RA. Immunohistochemical staining of synovial tissue showed abundant expression of MMP-9 by synovial tissue mast cells in patients with RA but not in normal controls. The expression, activity, and production of MMP-9 in mast cells was confirmed by RT-PCR, zymography, and Western blotting using cord blood-derived human mast cells (CB-HMC). Treatment of CB-HMC with TNF-α significantly increased the expression of MMP-9 mRNA and up-regulated the activity of MMP-9 in a time- and dose-dependent manner. By contrast, IFN-γ inhibited MMP-9 mRNA and protein expression. The cytokine-mediated regulation of MMP-9 was also apparent in the human mast cell line (HMC-1) and in mouse bone marrow-derived mast cells. Furthermore, TNF-α significantly increased the invasiveness of CB-HMC across Matrigel-coated membranes while the addition of IFN-γ, rTIMP-1, or pharmacological MMP inhibitors significantly reduced this process. These observations suggest that MMP-9 is not a stored product in mast cells but these cells are capable of producing this enzyme under inflammatory conditions that may facilitate the migration of mast cell progenitors to sites of inflammation and may also contribute to local tissue damage.

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“…Large quantities of tryptase in the BF, brain and other organs (which was absent in negative control) indicated that it may be involved in inflammation. Tryptase is the most abundant product of the MCs and it's quantity is directly related to the number of MCs (Wang et al, 2009a) and it can stimulate MCs secretion, causing a feedback cycle as the disease progresses (He et al, 1998). Degranulated MCs release tryptase that may then attract neighbouring MCs, leading to inflammation and lesions (Wang et al, 2009a).…”

Section: Mast Cellsmentioning

confidence: 99%

Interaction of infectious bursal disease virus with the immune system of poultry

Rehman

Chen

Umar

et al. 2016

World's Poultry Science Journal

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Immune dysfunction can be either at the humoral or cellular levels and is mediated by a myriad of factors including virus-induced immunosuppression. Infectious bursal disease virus (IBDV) affects domesticated poultry and causing health problems mainly due to prolonged immunosuppression. Destruction of the immunoglobulin-producing cells is the principal cause of IBDV-induced immunosuppression, which leads to significant impairment of the primary antibody responses. Due to these effects, IBDV infection not only increases the susceptibility of poultry to other viral infections but predisposes the host to several other bacteria of variable pathologies. The IBDV-induced immunesuppression is well-known phenomenon, however, recently there have been significant advancements in understanding the molecular mechanisms of this immune-suppression. This review discuss current updates regarding the immunotoxic and immunosuppressive nature of IBDV in the poultry and highlights areas requiring future research attentions that may help to establish foundations for effective and improved vaccines against IBDV.

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The activation of synovial mast cells: modulation of histamine release by tryptase and chymase and their inhibitors

Cited by 101 publications

References 28 publications

Modulation of tryptase secretion from human colon mast cells by histamine

Modulation of tryptase secretion from human colon mast cells by histamine

Human Mast Cell-Derived Gelatinase B (Matrix Metalloproteinase-9) Is Regulated by Inflammatory Cytokines: Role in Cell Migration

Interaction of infectious bursal disease virus with the immune system of poultry

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