Inductions of Histidine Decarboxylase in Mouse Tissues following Systemic Antigen Challenge: Contributions Made by Mast Cells, Non-Mast Cells and IL-1

2007 ◽  
Vol 144 (1) ◽  
pp. 69-78 ◽  
Author(s):  
Xue Deng ◽  
Xia Wu ◽  
Zhiqian Yu ◽  
Iwao Arai ◽  
Takashi Sasano ◽  
...  
Keyword(s):  
Mast Cells ◽  
Histidine Decarboxylase ◽  
Antigen Challenge ◽  
Mouse Tissues

scholarly journals Immunoglobulin E plus antigen challenge induces a novel intercrine/chemokine in mouse mast cells.

1992 ◽  
Vol 176 (6) ◽  
pp. 1773-1778 ◽  
Author(s):  
P A Kulmburg ◽  
N E Huber ◽  
B J Scheer ◽  
M Wrann ◽  
T Baumruker
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Immunoglobulin E ◽  
Late Phase ◽  
Antigen Challenge ◽  
Pcr Analysis ◽  
Phase Reaction ◽  
Late Phase Reaction ◽  
Mouse Tissues ◽  
Peritoneal Mast Cells

In an attempt to characterize genes participating in the allergic late phase reaction, we have isolated a novel intercrine/chemokine (called MARC) from a cDNA library of the stimulated mouse mast cell line, CPII. As measured by Northern blotting, it is strongly upregulated at the mRNA level after the physiological challenge of the cells with immunoglobulin (Ig)E plus antigen. Unstimulated cells completely lack significant, stable expression, as do a number of other, different cell lines (uninduced and induced) and mouse tissues. In contrast to the Northern blot analysis, a polymerase chain reaction (PCR) analysis, performed on CPII cells and on Percoll gradient purified mouse peritoneal mast cells, revealed a basal level of transcription in the uninduced stage. After 2 h of IgE plus antigen challenge, a quantitative reverse transcriptase-PCR, using a spiked in MIMIC, showed a level of transcripts more than 100-fold higher in the CPII cells and 5-20-fold higher in purified mouse peritoneal cavity mast cells. This rapid induction after the Fc epsilon RI challenge, the identification of the gene as a member of the chemokine family, and its upregulated expression in peritoneal mast cells, all suggest an involvement in certain acute and chronic pathological mast cell-driven diseases.

Mast cells and histamine concentration in muscle and liver of dystrophic mice

1964 ◽  
Vol 206 (2) ◽  
pp. 338-340 ◽  
Author(s):  
Pierre Bois
Keyword(s):  
Mast Cells ◽  
Histidine Decarboxylase ◽  
Binding Capacity ◽  
The Other ◽  
Decarboxylase Activity ◽  
Histamine Concentration ◽  
Other Hand ◽  
Histamine Binding ◽  
Dystrophic Mice ◽  
Histidine Decarboxylase Activity

The distribution of mast cells in muscle and liver of dystrophic mice was studied; histamine and histidine decarboxylase activity was also measured in the same tissues. Mast cells were significantly more numerous in dystrophic muscles. On the other hand, very few cells could be counted in the liver of either control or dystrophic animals. Histamine concentration was higher in muscle and liver of dystrophic mice; no visible increase in histidine decarboxylase activity could be measured by the methods used. It is concluded that histamine-binding capacity is increased in some tissues of dystrophic mice.

scholarly journals Effect of α-fluoromethy1 histidine, a suicide inhibitor of histidine decarboxylase, on histamine content of mouse tissues

1981 ◽  
Vol 31 ◽  
pp. 87
Author(s):  
Kazutaka Maeyama ◽  
Takehiko Watanabe ◽  
Yoshitaka Taguchi ◽  
Atsushi Yamatodani ◽  
Takuma Furitsu ◽  
...  
Keyword(s):  
Histidine Decarboxylase ◽  
Histamine Content ◽  
Mouse Tissues

Kinetics of protein phosphorylation and mediator secretion following antigen challenge of mast cells sensitized with monoclonal IgE or with reaginic serum

1997 ◽  
Vol 46 (13) ◽  
pp. 21-22
Author(s):  
C. Guérin-Marchand ◽  
T. Michon ◽  
B. Kolago ◽  
F. Marchand ◽  
A. Weyer ◽  
...  
Keyword(s):  
Mast Cells ◽  
Protein Phosphorylation ◽  
Antigen Challenge ◽  
Mediator Secretion ◽  
Kinetics Of

Increase in histidine decarboxylase activity of rat skin following treatment with compound 48/80

1959 ◽  
Vol 196 (2) ◽  
pp. 295-298 ◽  
Author(s):  
Richard W. Schayer ◽  
Zuleika Rothschild ◽  
Piroska Bizony
Keyword(s):  
Mast Cells ◽  
Histidine Decarboxylase ◽  
Probable Mechanism ◽  
Decarboxylase Activity ◽  
Rat Skin ◽  
Duration Of Treatment ◽  
Histological Studies ◽  
Histamine Liberator ◽  
Histidine Decarboxylase Activity ◽  
Intact Rats

Repeated injections of rats with compound 48/80, a histamine liberator, results in a marked increase in histidine decarboxylase activity of the skin. The increase is roughly proportional to the duration of treatment. This eliminates activation of pre-existing histidine decarboxylase as a probable mechanism. The increase can be demonstrated in intact rats; therefore, rat skin histidine decarboxylase is an adaptive enzyme. It seems probable that 48/80 treatment leads to the production of new, resistant mast cells which are particularly active in forming histamine. This speculation is compatible with reports from other laboratories of histological studies on rats given 48/80. Implications of this finding are discussed.

Histidine Decarboxylase (HDC) as Novel Marker of Immature Neoplastic Mast Cells in Systemic Mastocytosis.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4755-4755
Author(s):  
Maria T. Krauth ◽  
Hermine Agis ◽  
Karl J. Aichberger ◽  
Ingrid Simonitsch ◽  
Leonhard Muellauer ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Progenitor Cells ◽  
Histidine Decarboxylase ◽  
Systemic Mastocytosis ◽  
Bone Marrow Involvement ◽  
Hematopoietic Progenitor Cells ◽  
Pcr Analysis ◽  
Maturation Stage ◽  
Hematopoietic Progenitor

Abstract Synthesis of histamine in hematopoietic progenitor cells may be one of the earliest events in mast cell-development from pluripotent hematopoietic progenitor cells. In the present study, we asked whether the key enzyme involved in histamine generation, histidine decarboxylase (HDC), can be employed as an immunohistochemical marker for the detection of (neoplastic) mast cells (MC) in patients with cutaneous (CM) or systemic mastocytosis (SM). To address this question, we examined bone marrow biopsy specimens in a cohort of 101 patients (CM, n=10; indolent SM, n=46; SM with associated clonal non-MC lineage disease, n=31; aggressive SM, n=10; MC leukemia, n=3; MC sarcoma, n=1) using an antibody against HDC. Independent of the maturation stage of MC or subtype of disease, the anti-HDC antibody produced clear diagnostic staining results in all patients with bone marrow involvement examined including those with MC leukemia and MC sarcoma, in which MC are particularly immature and often escape analysis when examined by conventional stains. In these patients (MC leukemia, n=2; MC sarcoma, n=1), expression of HDC was reconfirmed at the mRNA level by RT-PCR analysis performed with RNA of highly enriched sorted CD117+ MC. In patients with CM or normal/reactive bone marrow (n=30), no HDC-positive infiltrates were detected. In these patients, only a few hematopoietic cells, presumably basophils, were found to react with the anti-HDC antibody. In summary, HDC is expressed in neoplastic bone marrow MC in patients with SM independent of the maturation stage of cells or the variant of disease. HDC should therefore be considered as a new MC marker in the screen panel of antigens employed to diagnose high grade MC malignancies.

Comparison of the Expression of Histidine Decarboxylase and Tryptase in Human Skin Mast Cells, Monocytes and Macrophages

2001 ◽  
Vol 124 (1-3) ◽  
pp. 158-159
Author(s):  
Ruth Schiffer ◽  
Jens M. Baron ◽  
Katja Belke ◽  
Ursula Braam ◽  
Hans F. Merk ◽  
...  
Keyword(s):  
Mast Cells ◽  
Human Skin ◽  
Histidine Decarboxylase ◽  
Monocytes And Macrophages

scholarly journals Increased acid responsiveness in vagal sensory neurons in a guinea pig model of eosinophilic esophagitis

2014 ◽  
Vol 307 (2) ◽  
pp. G149-G157 ◽  
Author(s):  
Youtian Hu ◽  
Zhenyu Liu ◽  
Xiaoyun Yu ◽  
Pankaj J. Pasricha ◽  
Bradley J. Undem ◽  
...  
Keyword(s):  
Mast Cells ◽  
Guinea Pig ◽  
Eosinophilic Esophagitis ◽  
Sensory Nerve ◽  
Pig Model ◽  
Antigen Challenge ◽  
Esophageal Wall ◽  
Patch Clamp Recording ◽  
Peripheral Tissues ◽  
Guinea Pig Model

Eosinophilic esophagitis (EoE) is characterized with eosinophils and mast cells predominated allergic inflammation in the esophagus and present with esophageal dysfunctions such as dysphagia, food impaction, and heartburn. However, the underlying mechanism of esophageal dysfunctions is unclear. This study aims to determine whether neurons in the vagal sensory ganglia are modulated in a guinea pig model of EoE. Animals were actively sensitized by ovalbumin (OVA) and then challenged with aerosol OVA inhalation for 2 wk. This results in a mild esophagitis with increases in mast cells and eosinophils in the esophageal wall. Vagal nodose and jugular neurons were disassociated, and their responses to acid, capsaicin, and transient receptor potential vanilloid type 1 (TRPV1) antagonist AMG-9810 were studied by calcium imaging and whole cell patch-clamp recording. Compared with naïve animals, antigen challenge significantly increased acid responsiveness in both nodose and jugular neurons. Their responses to capsaicin were also increased after antigen challenge. AMG-9810, at a concentration that blocked capsaicin-evoked calcium influx, abolished the increase in acid-induced activation in both nodose and jugular neurons. Vagotomy strongly attenuated those increased responses of nodose and jugular neurons to both acid and capsaicin induced by antigen challenge. These data for the first time demonstrated that prolonged antigen challenge significantly increases acid responsiveness in vagal nodose and jugular ganglia neurons. This sensitization effect is mediated largely through TRPV1 and initiated at sensory nerve endings in the peripheral tissues. Allergen-induced enhancement of responsiveness to noxious stimulation by acid in sensory nerve may contribute to the development of esophageal dysfunctions such as heartburn in EoE.

Relationship of the number of mast cells and the activity of histidine decarboxylase (HDC)

1994 ◽  
Vol 8 (1) ◽  
pp. 85
Author(s):  
H. Minami ◽  
K. Sato ◽  
H. Taguchi ◽  
T. Maeda ◽  
K. Yoshikawa
Keyword(s):  
Mast Cells ◽  
Histidine Decarboxylase ◽  
Relationship Of
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