Mast Cell-Eosinophil-Fibroblast Crosstalk in Allergic Inflammation

2000 ◽  
pp. 81-92 ◽  
Author(s):  
S.J. Smith ◽  
F. Levi-Schaffer
Keyword(s):  
Mast Cell ◽  
Allergic Inflammation

scholarly journals GATA2 regulates mast cell identity and responsiveness to antigenic stimulation by promoting chromatin remodeling at super-enhancers

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yapeng Li ◽  
Junfeng Gao ◽  
Mohammad Kamran ◽  
Laura Harmacek ◽  
Thomas Danhorn ◽  
...  
Keyword(s):  
Mast Cell ◽  
Binding Sites ◽  
Cell Lineage ◽  
Allergic Inflammation ◽  
Chromatin Accessibility ◽  
Antigenic Stimulation ◽  
Parasitic Infections ◽  
Cell Identity ◽  
Super Enhancer ◽  
Determining Factors

AbstractMast cells are critical effectors of allergic inflammation and protection against parasitic infections. We previously demonstrated that transcription factors GATA2 and MITF are the mast cell lineage-determining factors. However, it is unclear whether these lineage-determining factors regulate chromatin accessibility at mast cell enhancer regions. In this study, we demonstrate that GATA2 promotes chromatin accessibility at the super-enhancers of mast cell identity genes and primes both typical and super-enhancers at genes that respond to antigenic stimulation. We find that the number and densities of GATA2- but not MITF-bound sites at the super-enhancers are several folds higher than that at the typical enhancers. Our studies reveal that GATA2 promotes robust gene transcription to maintain mast cell identity and respond to antigenic stimulation by binding to super-enhancer regions with dense GATA2 binding sites available at key mast cell genes.

The Role of the Mast Cell in Acute and Chronic Allergic Inflammation

1994 ◽  
Vol 725 (1) ◽  
pp. 13-21 ◽  
Author(s):  
MARTIN K. CHURCH ◽  
YOSHIMICHI OKAYAMA ◽  
PETER BRADDING
Keyword(s):  
Mast Cell ◽  
Allergic Inflammation

Effect of Chicoric Acid on Mast Cell-Mediated Allergic Inflammation in Vitro and in Vivo

2015 ◽  
Vol 78 (12) ◽  
pp. 2956-2962 ◽  
Author(s):  
Na Young Lee ◽  
Kyung-Sook Chung ◽  
Jong Sik Jin ◽  
Keuk Soo Bang ◽  
Ye-Jin Eom ◽  
...  
Keyword(s):  
Mast Cell ◽  
Allergic Inflammation ◽  
Chicoric Acid

scholarly journals Roxatidine attenuates mast cell-mediated allergic inflammation via inhibition of NF-κB and p38 MAPK activation

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Minho Lee ◽  
Na Young Lee ◽  
Kyung-Sook Chung ◽  
Se-Yun Cheon ◽  
Kyung-Tae Lee ◽  
...  
Keyword(s):  
Mast Cell ◽  
P38 Mapk ◽  
Allergic Inflammation ◽  
Mapk Activation

Nothofagin suppresses mast cell-mediated allergic inflammation

2019 ◽  
Vol 298 ◽  
pp. 1-7 ◽  
Author(s):  
Byeong-Cheol Kang ◽  
Min-Jong Kim ◽  
Soyoung Lee ◽  
Young-Ae Choi ◽  
Pil-Hoon Park ◽  
...  
Keyword(s):  
Mast Cell ◽  
Allergic Inflammation

scholarly journals Divergent effects of acute and prolonged interleukin 33 exposure on mast cell IgE-mediated functions

2018 ◽  
Author(s):  
Elin Rönnberg ◽  
Avan Ghaib ◽  
Carlos Ceriol ◽  
Mattias Enoksson ◽  
Michel Arock ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Prolonged Exposure ◽  
Allergic Inflammation ◽  
Acute Effect ◽  
Receptor Expression ◽  
Human Mast Cell ◽  
Interleukin 33 ◽  
Cell Functions ◽  
Ige Mediated

AbstractBackgroundEpithelial cytokines, including IL-33 and TSLP, have attracted interest because of their roles in chronic allergic inflammation-related conditions such as asthma. Mast cells are one of the major targets of IL-33, to which they respond by secreting cytokines. Most studies performed thus far have investigated the acute effects of IL-33 on mast cells.ObjectiveThe objective of this study is to investigate how acute versus prolonged exposure of human mast cells to IL-33 and TSLP affects mediator synthesis and IgE-mediated activation.MethodsHuman lung mast cells (HLMCs), cord blood-derived mast cells (CBMCs), and the ROSA mast cell line were used for this study. Surface receptor expression and the levels of mediators were measured after treatment with IL-33 and/or TSLP.ResultsIL-33 induced the acute release of cytokines. Prolonged exposure to IL-33 increased while TSLP reduced intracellular levels of tryptase. Acute IL-33 treatment strongly potentiated IgE-mediated activation. In contrast, four days of exposure to IL-33 decreased IgE-mediated activation, an effect that was accompanied by a reduction in FcεRI expression.Conclusion & Clinical RelevanceWe show that IL-33 plays dual roles for mast cell functions. The acute effect includes cytokine release and the potentiation of IgE-mediated degranulation, whereas prolonged exposure to IL-33 reduces IgE-mediated activation. We conclude that mast cells act quickly in response to the alarmin IL-33 to initiate an acute inflammatory response, whereas extended exposure to IL-33 during prolonged inflammation reduces IgE-mediated responses. This negative feedback effect suggests the presence of a novel IL-33 mediated regulatory pathway that modulates IgE-induced human mast cell responses.

Inhibitory effects of orientin in mast cell-mediated allergic inflammation

2020 ◽  
Vol 72 (4) ◽  
pp. 1002-1010
Author(s):  
Hima Dhakal ◽  
Soyoung Lee ◽  
Jin Kyeong Choi ◽  
Taeg Kyu Kwon ◽  
Dongwoo Khang ◽  
...  
Keyword(s):  
Mast Cell ◽  
Allergic Inflammation ◽  
Inhibitory Effects

Inhibitory Effect of Retinoic Acid on Proliferation, Maturation and Tryptase Level in Human Leukemic Mast Cells (HMC-1)

2003 ◽  
Vol 16 (1) ◽  
pp. 43-47 ◽  
Author(s):  
M.G. Alexandrakis ◽  
D.S. Kyriakou ◽  
D. Seretakis ◽  
W. Boucher ◽  
R. Letourneau ◽  
...  
Keyword(s):  
Mast Cell ◽  
Retinoic Acid ◽  
Mast Cells ◽  
Allergic Inflammation ◽  
Inhibitory Effect ◽  
Control Group ◽  
Tryptase Level ◽  
Synthetic Derivatives ◽  
Derivatives Of ◽  
Inhibit Cell Proliferation

Mast cells play an important role in allergic inflammation by releasing histamine, tryptase and several inflammatory cytokines. Human leukemic mast cells (HMC-1) have been used to study mast cell mediators and their role in inflammatory mechanisms. HMC-1 contain and release several inflammatory mediators, of which the proteolytic enzyme tryptase is most characteristic. Retinoids, including retinoic acid, are naturally occurring and synthetic derivatives of vitamin A. All-trans-retinoic (ATRA) acid had been previously reported to inhibit cell proliferation, differentiation and apoptosis. In the present study, we investigated the effect of ATRA on the proliferation and secretion of tryptase in HMC-1. HMC-1 were treated with ATRA at 10-4M, 10-5M or 10-6M for 3,4 or 5 days in culture. Control HMC-1 were treated with equal amount of culture medium only. ATRA decreased the number of HMC-1 as compared to the control group. The same treatment for 3, 4 or 5 days also decreased intracellular tryptase levels. These results indicate that ATRA significantly inhibits both proliferation and growth as shown by the decreased intracellular tryptase levels in HMC-1. ATRA may be a useful agent in the treatment of mast cell proliferative disorders.

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