Corrigendum to “Antiallergic effect of KOB03, a polyherbal medicine, on mast cell-mediated allergic responses in ovalbumin-induced allergic rhinitis mouse and human mast cells” [J. Ethnopharmacol. 142(3) (2012) 684–693]

Abstract Nerve growth factor (NGF ) can influence mast cell development and function in murine rodents by interacting with its receptors on mast cells. We now report the identification of mRNA transcripts of full-length tyrosine kinase-containing trkA, trkB, and trkC neurotrophin receptor genes in HMC-1 human mast cell leukemia cells. Although HMC-1 cells lacked p75 mRNA, they expressed transcripts for the exon-lacking splice variant of trkA (trkAI), truncated trkB (trkB.T1), and truncated trkC. By flow cytometry, HMC-1 cells exhibited expression of TrkA, TrkB, and TrkC receptor proteins containing full-length tyrosine kinase domains. NGF stimulation of HMC-1 cells induced tyrosine phosphorylation of TrkA protein, increased expression of the early response genes c-fos and NGF1-A, and activation of ERK-mitogen–activated protein (MAP) kinase, results which indicate that TrkA receptors in HMC-1 cells are fully functional. Highly purified populations of human lung mast cells expressed mRNAs for trkA, trkB and trkC, whereas preparations of human umbilical cord blood-derived mast cells expressed mRNAs for trkA and trkC, but not trkB. Moreover, preparations of human umbilical cord blood-derived immature mast cells not only expressed mRNA transcript and protein for TrkA, but exhibited significantly higher numbers of chymase-positive cells after the addition of NGF to their culture medium for 3 weeks. In addition, HMC-1 cells expressed mRNAs for NGF, brain-derived neurotrophic factor (BDNF ), and neurotrophin-3 (NT-3), the cognate ligands for TrkA, TrkB, and TrkC, whereas NGF and BDNF transcripts were detectable in human umbilical cord blood mast cell preparations. Taken together, our findings show that human mast cells express a functional TrkA receptor tyrosine kinase and indicate that NGF may be able to promote certain aspects of mast cell development and/or maturation in humans. Our studies also raise the possibility that human mast cells may represent a potential source for neurotrophins.

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Histamine release from rodent and human mast cells induced by protoporphyrin and ultraviolet light: studies of the mechanism of mast-cell activation in erythropoietic protoporphyria

British Journal of Dermatology ◽

10.1111/j.1365-2133.1990.tb14727.x ◽

1990 ◽

Vol 122 (4) ◽

pp. 501-512 ◽

Cited By ~ 22

Author(s):

RENEE A. GLOVER ◽

CYNTHIA S. BAILEY ◽

KIM E. BARRETT ◽

S.I. WASSERMAN ◽

IRMA GIGLI

Keyword(s):

Mast Cell ◽

Mast Cells ◽

Histamine Release ◽

Ultraviolet Light ◽

Cell Activation ◽

Mast Cell Activation ◽

Erythropoietic Protoporphyria ◽

Human Mast Cells

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SNAP23-Dependent Surface Translocation of Leukotriene B4 (LTB4) Receptor 1 Is Essential for NOX2-Mediated Exocytotic Degranulation in Human Mast Cells Induced by Trichomonas vaginalis-Secreted LTB4

Infection and Immunity ◽

10.1128/iai.00526-16 ◽

2016 ◽

Vol 85 (1) ◽

Cited By ~ 1

Author(s):

Arim Min ◽

Young Ah Lee ◽

Kyeong Ah Kim ◽

Jamel El-Benna ◽

Myeong Heon Shin

Keyword(s):

Mast Cell ◽

Mast Cells ◽

Trichomonas Vaginalis ◽

Cell Activation ◽

Mast Cell Activation ◽

Ros Generation ◽

Physical Interaction ◽

Content Type ◽

Receptor Complexes ◽

Human Mast Cells

ABSTRACT Trichomonas vaginalis is a sexually transmitted parasite that causes vaginitis in women and itself secretes lipid mediator leukotriene B4 (LTB4). Mast cells are important effector cells of tissue inflammation during infection with parasites. Membrane-bridging SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complexes are critical for fusion during exocytosis. Although T. vaginalis-derived secretory products (TvSP) have been shown to induce exocytosis in mast cells, information regarding the signaling mechanisms between mast cell activation and TvSP is limited. In this study, we found that SNAP23-dependent surface trafficking of LTB4 receptor 1 (BLT1) is required for nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2)-mediated exocytotic degranulation of mast cells induced by TvSP. First, stimulation with TvSP induced exocytotic degranulation and reactive oxygen species (ROS) generation in HMC-1 cells. Next, TvSP-induced ROS generation and exocytosis were strongly inhibited by transfection of BLT1 small interfering RNA (siRNA). TvSP induced trafficking of BLT1 from the cytosol to the plasma membrane. We also found that knockdown of SNAP23 abrogated TvSP-induced ROS generation, exocytosis, and surface trafficking of BLT1 in HMC-1 cells. By coimmunoprecipitation, there was a physical interaction between BLT1 and SNAP23 in TvSP-stimulated HMC-1 cells. Taken together, our results suggest that SNAP23-dependent surface trafficking of BLT1 is essential for exocytosis in human mast cells induced by T. vaginalis-secreted LTB4. Our data collectively demonstrate a novel regulatory mechanism for SNAP23-dependent mast cell activation of T. vaginalis-secreted LTB4 involving surface trafficking of BLT1. These results can help to explain how the cross talk mechanism between parasite and host can govern deliberately tissue inflammatory responses.

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Regulatory effects of stem cell factor and interleukin-4 on adhesion of human mast cells to extracellular matrix proteins

Blood ◽

10.1182/blood.v99.3.966 ◽

2002 ◽

Vol 99 (3) ◽

pp. 966-972 ◽

Cited By ~ 47

Author(s):

Axel Lorentz ◽

Detlef Schuppan ◽

Andreas Gebert ◽

Michael P. Manns ◽

Stephan C. Bischoff

Keyword(s):

Extracellular Matrix ◽

Mast Cell ◽

Stem Cell ◽

Cell Adhesion ◽

Mast Cells ◽

Stem Cell Factor ◽

Collagen I ◽

Interleukin 4 ◽

Human Mast Cells ◽

Ecm Proteins

Abstract Mast cells are inflammatory and immunoregulatory cells resident in tissues. They develop from bone marrow-derived progenitor cells that enter the tissue through the blood circulation. The specific localization and migration of mast cells in tissues is dependent on their interaction with extracellular matrix (ECM) proteins. Adhesion of human mast cells isolated from intestinal mucosa and cultured in the presence of stem cell factor (SCF) to ECM proteins is analyzed. It was observed that SCF is a unique cytokine enhancing mast cell adhesion to all tested ECM proteins (fibronectin, laminin, collagen I, III, IV, VI, XIV) up to 5-fold, particularly to fibronectin (54% ± 12% of mast cells) and to denatured collagens (40% ± 12% on cyanogen bromide-cleaved peptides of collagen I). Most noteworthy, preculture of mast cells with interleukin-4 (IL-4), in addition to SCF, reduced their potency to adhere to ECM proteins to one third compared to mast cells cultured with SCF alone. Mast cell adhesion was preferentially mediated by β1 integrins, and most cells expressed the ECM-binding integrins α2β1, α3β1, α4β1, α5β1, and αVβ3. SCF-induced mast cell adhesion was totally blocked by wortmannin and apigenin, indicating an involvement of phosphatidylinositol 3-kinase and mitogen-activated protein kinase, and it was related to an up-regulation of the HUTS-21 β1 epitope, which is associated with an activated conformation of β1. In conclusion, these data indicate that SCF induces the adhesion of cultured mast cells to ECM proteins, whereas IL-4 may promote detachment from the ECM.

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Killer Immunoglobulin-Like Receptor 2DL4 (CD158d) Regulates Human Mast Cells Both Positively and Negatively: Possible Roles in Pregnancy and Cancer Metastasis

10.20944/preprints201910.0331.v1 ◽

2019 ◽

Author(s):

Tatsuki R. Kataoka ◽

Chiyuki Ueshima ◽

Masahiro Hirata ◽

Sachiko Minamiguchi ◽

Hironori Haga

Keyword(s):

Mast Cell ◽

Mast Cells ◽

Cancer Metastasis ◽

Nk Cell ◽

Human Leukocyte ◽

Human Mast Cell ◽

Allergic Reactions ◽

Ige Receptor ◽

Human Mast Cells ◽

In Pregnancy

Killer immunoglobulin-like receptor (KIR) 2DL4 (CD158d) was previously thought to be a human NK-cell-specific protein but its expression has also been demonstrated in human mast cells. Mast cells are involved in allergic reactions via their KIT-mediated and IgE receptor-mediated responses. We recently detected the expression of KIR2DL4 in human cultured mast cells established from peripheral blood derived from healthy volunteers (PB-mast), a human mast cell line (LAD2), and non-neoplastic mast cells, including pathological specimens. An agonistic antibody against KIR2DL4 negatively regulates the KIT- and IgE-receptor-mediated responses of PB-mast and LAD2 cells. In addition, agonistic antibodies and human leukocyte antigen (HLA)-G, a natural ligand for KIR2DL4, induce the secretion from these cells of leukemia inhibitory factor and serine proteases, which have been implicated in pregnancy establishment and cancer metastasis. Therefore, KIR2DL4 stimulation with agonistic antibodies and recombinant HLA-G protein may enhance both processes, in addition to suppressing mast-cell-mediated allergic reactions.

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The Inferior Turbinate Mast Cell Population of Patients with Perennial Allergic and Nonallergic Rhinitis

American Journal of Rhinology ◽

10.2500/105065897781446775 ◽

1997 ◽

Vol 11 (1) ◽

pp. 63-66 ◽

Cited By ~ 31

Author(s):

Gilead Berger ◽

Arnon Goldberg ◽

Dov Ophir

Keyword(s):

Allergic Rhinitis ◽

Mast Cell ◽

Mast Cells ◽

Inferior Turbinate ◽

Blue Staining ◽

Perennial Allergic Rhinitis ◽

Nonallergic Rhinitis ◽

Cell Counts ◽

Significant Difference ◽

Normal Controls

The number of mast cells in the inferior turbinates of patients with perennial allergic rhinitis and perennial nonallergic rhinitis was compared with normal controls. Mast cell counts expressed as the mean number in 100 high-power fields, assessed after Carnoy's fixation and toluidine blue staining were 1.84 in normal controls (n = 11), 4.39 in patients with perennial allergic rhinitis (n = 13), and 4.00 in those with perennial nonallergic rhinitis (n = 26). Statistical analysis confirmed that the density of mast cells in allergic as well as in nonallergic patients was significantly higher than in normal controls, whereas no significant difference was found between the number of mast cells in allergic and nonallergic patients. It is concluded that the number of mast cells in the inferior turbinate mucosa of patients with perennial rhinitis is increased compared with normal controls, and the increased number is not necessarily allergy-dependent.

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Dengue Virus Selectively Induces Human Mast Cell Chemokine Production

Journal of Virology ◽

10.1128/jvi.76.16.8408-8419.2002 ◽

2002 ◽

Vol 76 (16) ◽

pp. 8408-8419 ◽

Cited By ~ 110

Author(s):

Christine A. King ◽

Robert Anderson ◽

Jean S. Marshall

Keyword(s):

Mast Cell ◽

Mast Cells ◽

Virus Infection ◽

Dengue Virus ◽

Specific Antibody ◽

Human Mast Cell ◽

Dengue Virus Infection ◽

Human Mast Cells ◽

Virus Specific Antibody ◽

Rantes Production

ABSTRACT Severe dengue virus infections usually occur in individuals who have preexisting anti-dengue virus antibodies. Mast cells are known to play an important role in host defense against several pathogens, but their role in viral infection has not yet been elucidated. The effects of dengue virus infection on the production of chemokines by human mast cells were examined. Elevated levels of secreted RANTES, MIP-1α, and MIP-1β, but not IL-8 or ENA-78, were observed following infection of KU812 or HMC-1 human mast cell-basophil lines. In some cases a >200-fold increase in RANTES production was observed. Cord blood-derived cultured human mast cells treated with dengue virus in the presence of subneutralizing concentrations of dengue virus-specific antibody also demonstrated significantly (P < 0.05) increased RANTES production, under conditions which did not induce significant degranulation. Chemokine responses were not observed when mast cells were treated with UV-inactivated dengue virus in the presence or absence of human dengue virus-specific antibody. Neither antibody-enhanced dengue virus infection of the highly permissive U937 monocytic cell line nor adenovirus infection of mast cells induced a RANTES, MIP-1α, or MIP-1β response, demonstrating a selective mast cell response to dengue virus. These results suggest a role for mast cells in the initiation of chemokine-dependent host responses to dengue virus infection.

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