Mediator Release from Human Lung Mast Cells

2015 ◽  
pp. 64-73 ◽  
Author(s):  
S. T. Holgate ◽  
R. C. Benyon ◽  
M. K. Church
Keyword(s):  
Mast Cells ◽  
Human Lung ◽  
Mediator Release

Effect of the c-kit Ligand on Mediator Release by Human Lung Mast Cells

1992 ◽  
Vol 99 (2-4) ◽  
pp. 319-322 ◽  
Author(s):  
Stephan C. Bischoff ◽  
Clemens A. Dahinden
Keyword(s):  
Mast Cells ◽  
Human Lung ◽  
Mediator Release

Adenosine Potentiates Mediator Release from Human Lung Mast Cells

1988 ◽  
Vol 138 (5) ◽  
pp. 1143-1151 ◽  
Author(s):  
Peter T. Peachell ◽  
Michele Columbo ◽  
Anne Kagey-Sobotka ◽  
Lawrence M. Lichtenstein ◽  
Gianni Marone
Keyword(s):  
Mast Cells ◽  
Human Lung ◽  
Mediator Release

Relationship between Mediator Release from Human Lung Mast Cells in vitro and in vivo

1985 ◽  
Vol 77 (1-2) ◽  
pp. 47-56 ◽  
Author(s):  
S.T. Holgate ◽  
R.C. Benyon ◽  
P.H. Howarth ◽  
R. Agius ◽  
C. Hardy ◽  
...  
Keyword(s):  
Mast Cells ◽  
Human Lung ◽  
Mediator Release

scholarly journals c-kit ligand: a unique potentiator of mediator release by human lung mast cells.

1992 ◽  
Vol 175 (1) ◽  
pp. 237-244 ◽  
Author(s):  
S C Bischoff ◽  
C A Dahinden
Keyword(s):  
Growth Factor ◽  
Mast Cells ◽  
Cell Growth ◽  
Human Lung ◽  
Immunoglobulin E ◽  
Mediator Release ◽  
Ige Receptor ◽  
Effector Cells ◽  
Promote Cell Proliferation ◽  
Kit Ligand

Mast cells (MC) play a central role in extrinsic allergic reactions such as asthma and may participate in other inflammatory and fibrotic processes. However, with the exception of immunoglobulin E (IgE) receptor-dependent stimulation, no secretagogues of human lung MC have yet been described. It is also unclear whether mediator release can be regulated by certain cytokines as demonstrated previously in basophils and other human inflammatory effector cells. Here, we show that the c-kit ligand (KL), a recently identified stem cell growth factor, at concentrations 10-100 times lower than that required to promote cell proliferation, enhances the release of histamine and leukotriene C4 in response to IgE receptor crosslinking of human lung MC. KL does not induce mediator release per se, but increases the sensitivity of MC to anti-IgE receptor stimulation and also enhances mediator release to maximally effective concentrations of anti-IgE receptor antibody. By contrast, a large number of cytokines examined, including the mast cell growth factors/agonists in rodents, interleukin 3 (IL-3), IL-4, IL-9, and nerve growth factor, were ineffective in this respect. These findings suggest a unique role of KL in regulating effector functions of human mucosal MC.

scholarly journals Effects of dexamethasone on mediator release from human lung fragments and purified human lung mast cells.

1983 ◽  
Vol 71 (6) ◽  
pp. 1830-1835 ◽  
Author(s):  
R P Schleimer ◽  
E S Schulman ◽  
D W MacGlashan ◽  
S P Peters ◽  
E C Hayes ◽  
...  
Keyword(s):  
Mast Cells ◽  
Human Lung ◽  
Mediator Release

scholarly journals Influence of islet-activating protein (IAP) on anaphylactic chemical mediator release from human lung fragments and mast cells

1992 ◽  
Vol 58 ◽  
pp. 118
Author(s):  
Takeshi Nabe ◽  
Hideki Yamamura ◽  
Shigekatsu Kohno ◽  
Joh Shindo ◽  
Michiaki Horiba ◽  
...  
Keyword(s):  
Mast Cells ◽  
Human Lung ◽  
Mediator Release ◽  
Chemical Mediator

scholarly journals Salmeterol inhibition of mediator release from human lung mast cells by β-adrenoceptor-dependent and independent mechanisms

1998 ◽  
Vol 123 (5) ◽  
pp. 1009-1015 ◽  
Author(s):  
Lee K. Chong ◽  
Elizabeth Cooper ◽  
Christopher J. Vardey ◽  
Peter T. Peachell
Keyword(s):  
Mast Cells ◽  
Human Lung ◽  
Mediator Release

scholarly journals The Contribution of Orai(CRACM)1 and Orai(CRACM)2 Channels in Store-Operated Ca2+ Entry and Mediator Release in Human Lung Mast Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e74895 ◽  
Author(s):  
Ian Ashmole ◽  
S. Mark Duffy ◽  
Mark L. Leyland ◽  
Peter Bradding
Keyword(s):  
Mast Cells ◽  
Human Lung ◽  
Mediator Release

scholarly journals IL-33 and Superantigenic Activation of Human Lung Mast Cells Induce the Release of Angiogenic and Lymphangiogenic Factors

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 145
Author(s):  
Leonardo Cristinziano ◽  
Remo Poto ◽  
Gjada Criscuolo ◽  
Anne Lise Ferrara ◽  
Maria Rosaria Galdiero ◽  
...  
Keyword(s):  
Mast Cells ◽  
Human Lung ◽  
Protein A ◽  
Protein L ◽  
Variable Regions ◽  
Prolonged Incubation ◽  
High Affinity ◽  
High Affinity Receptor ◽  
Affinity Receptor ◽  
Pleiotropic Functions

Human lung mast cells (HLMCs) express the high-affinity receptor FcεRI for IgE and are strategically located in different compartments of human lung, where they play a role in several inflammatory disorders and cancer. Immunoglobulin superantigens (e.g., protein A of Staphylococcus aureus and protein L of Peptostreptococcus magnus) bind to the variable regions of either the heavy (VH3) or light chain (κ) of IgE. IL-33 is a cytokine expressed by epithelial cells that exerts pleiotropic functions in the lung. The present study investigated whether immunoglobulin superantigens protein A and protein L and IL-33 caused the release of inflammatory (histamine), angiogenic (VEGF-A) and lymphangiogenic (VEGF-C) factors from HLMCs. The results show that protein A and protein L induced the rapid (30 min) release of preformed histamine from HLMCs. By contrast, IL-33 did not induce the release of histamine from lung mast cells. Prolonged incubation (12 h) of HLMCs with superantigens and IL-33 induced the release of VEGF-A and VEGF-C. Preincubation with IL-33 potentiated the superantigenic release of histamine, angiogenic and lymphangiogenic factors from HLMCs. Our results suggest that IL-33 might enhance the inflammatory, angiogenic and lymphangiogenic activities of lung mast cells in pulmonary disorders.

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