scholarly journals Rat peritoneal mast cells release dipeptidyl peptidase II

1986 ◽  
Vol 236 (1) ◽  
pp. 215-219 ◽  
Author(s):  
G Struckhoff ◽  
E Heymann
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Substance P ◽  
Peritoneal Lavage ◽  
Dipeptidyl Peptidase ◽  
Dependent Manner ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
Dose Dependent

Purified rat peritoneal mast cells have a 10-20-fold higher dipeptidyl peptidase II (DPP II) activity as compared with that of macrophages from the same source. Upon stimulation with the secretagogue Compound 48/80, DPP II is released from peritoneal-lavage cells and from purified mast cells, but not from purified macrophages, in a dose-dependent manner. Maximally, about one-third of the DPP II present in peritoneal-lavage cells is released. Substance P and the antigen/IgE system probably produce a similar effect. Both histamine and Zn2+, two ingredients of mast-cell granules, strongly inhibit DPP II at concentrations reported to occur in the granules. A possible role of mast-cell DPP II in the remodelling of connective tissue is discussed.

Inhibition of Mast Cell-Mediated Anaphylaxis by Sochungryong-Tang

2000 ◽  
Vol 28 (01) ◽  
pp. 69-76 ◽  
Author(s):  
H. M. Kim ◽  
G. S. Yoon ◽  
J. U. Seo ◽  
G. Moon ◽  
H. R. Kim ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Anaphylactic Shock ◽  
Mast Cell Degranulation ◽  
Dependent Manner ◽  
Asian Philosophy ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
Anti Body ◽  
Dose Dependent

According to traditional Asian philosophy, Sochungryong-Tang (S-Tang) is a prescription for treating exterior syndrome. In this study, we investigated the effect of S-Tang on mast cell-mediated anaphylaxis. S-Tang completely inhibited compound 48/80-induced systemic anaphylactic shock at a dose of 100 mg/kg. When S-Tang was given as pretreatment at concentrations ranging from 1 to 1000 mg/kg, the serum histamine levels induced by compound 48/80 were reduced in a dose-dependent manner. S-Tang inhibited the local anaphylaxis activated by anti-dinitrophenyl (DNP) IgE anti-body, and also inhibited the histamine release from the rat peritoneal mast cells by compound 48/80 or anti-DNP IgE. These results indicate that S-Tang may contain substances with actions that inhibit mast cell degranulation.

Effect of Alpinia oxyphylla Fruit Extract on Compound 48/80-induced Anaphylactic Reactions

2001 ◽  
Vol 29 (02) ◽  
pp. 293-302 ◽  
Author(s):  
Tae Yong Shin ◽  
Jin Hee Won ◽  
Hyung Min Kim ◽  
Sand Hyun Kim
Keyword(s):  
Mast Cells ◽  
Anaphylactic Shock ◽  
Dependent Manner ◽  
Basal Cells ◽  
Plasma Histamine ◽  
Fruit Extract ◽  
Alpinia Oxyphylla ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
Dose Dependent

The effect of the aqueous extract of Alpinia oxyphylla Miq. (Zingiberaceae) fruits (AOFE) on anaphylactic reaction was investigated. AOFE completely inhibited compound 48/80-induced systemic anaphylactic shock at dose of 1.0 g/kg. When AOFE was pretreated at concentrations ranging from 0.01 to 1.0 g/kg, the plasma histamine levels induced by compound 48/80 were reduced in a dose-dependent manner. AOFE also inhibited the histamine release from rat peritoneal mast cells (RPMC) by compound 48/80. The level of cAMP in RPMC, when AOFE was added, transiently and significantly increased about 4-fold compared with that of basal cells. These results indicate that AOFE may be beneficial in the treatment of non-specific anaphylactic reactions.

The transmembrane adaptor protein NTAL limits mast cell chemotaxis toward prostaglandin E2

2018 ◽  
Vol 11 (556) ◽  
pp. eaao4354 ◽  
Author(s):  
Ivana Halova ◽  
Monika Bambouskova ◽  
Lubica Draberova ◽  
Viktor Bugajev ◽  
Petr Draber
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
T Cell Activation ◽  
Cell Activation ◽  
Adaptor Protein ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
And Function ◽  
Cell Chemotaxis

Chemotaxis of mast cells is one of the crucial steps in their development and function. Non–T cell activation linker (NTAL) is a transmembrane adaptor protein that inhibits the activation of mast cells and B cells in a phosphorylation-dependent manner. Here, we studied the role of NTAL in the migration of mouse mast cells stimulated by prostaglandin E2 (PGE2). Although PGE2 does not induce the tyrosine phosphorylation of NTAL, unlike IgE immune complex antigens, we found that loss of NTAL increased the chemotaxis of mast cells toward PGE2. Stimulation of mast cells that lacked NTAL with PGE2 enhanced the phosphorylation of AKT and the production of phosphatidylinositol 3,4,5-trisphosphate. In resting NTAL-deficient mast cells, phosphorylation of an inhibitory threonine in ERM family proteins accompanied increased activation of β1-containing integrins, which are features often associated with increased invasiveness in tumors. Rescue experiments indicated that only full-length, wild-type NTAL restored the chemotaxis of NTAL-deficient cells toward PGE2. Together, these data suggest that NTAL is a key inhibitor of mast cell chemotaxis toward PGE2, which may act through the RHOA/ERM/β1-integrin and PI3K/AKT axes.

Role of common cytokine receptor γ chain (γc)– and Jak3-dependent signaling in the proliferation and survival of murine mast cells

Blood ◽  
2000 ◽  
Vol 96 (6) ◽  
pp. 2172-2180 ◽  
Author(s):  
Kotaro Suzuki ◽  
Hiroshi Nakajima ◽  
Norihiko Watanabe ◽  
Shin-ichiro Kagami ◽  
Akira Suto ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mast Cells ◽  
Cytokine Receptor ◽  
Type I ◽  
Dependent Manner ◽  
Type Ii ◽  
Wild Type ◽  
Peritoneal Mast Cells ◽  
The Common

Abstract The regulatory roles of the common cytokine receptor γ chain (γc)– and Jak3-dependent signaling in the proliferation and survival of mast cells were determined using γc-deficient (γc−) and Jak3-deficient (Jak3−) mice. Although the mast cells in γc− and Jak3− mice were morphologically indistinguishable from those in wild-type mice, the number of peritoneal mast cells was decreased in γc− and Jak3− mice as compared with that in wild-type mice. Among γc-related cytokines, interleukin (IL)-4 and IL-9, but not IL-2, IL-7, or IL-15, enhanced the proliferation and survival of bone marrow–derived mast cells (BMMCs) from wild-type mice. However, the effects of IL-4 and IL-9 were absent in BMMCs from γc− and Jak3−mice. In addition, IL-4Rα, γc, and Jak3, but not IL-2Rβ or IL-7Rα, were expressed in BMMCs. In contrast, IL-13 did not significantly induce the proliferation and survival of BMMCs even from wild-type mice, and IL-13Rα1 was not expressed in BMMCs. Furthermore, IL-4 phosphorylated the 65-kd isoform of Stat6 in BMMCs from wild-type mice but not from γc− and Jak3− mice. These results indicate that γc- and Jak3-dependent signaling is essential for IL-4– and IL-9–induced proliferation and survival of murine mast cells, that the effects of IL-4 are mediated by type I IL-4R and that type II IL-4R is absent on mast cells, and that IL-4 phosphorylates the 65-kd isoform of Stat6 in mast cells in a γc- and Jak3-dependent manner.

Role of nitric oxide in histamine release from human basophils and rat peritoneal mast cells

2001 ◽  
Vol 425 (3) ◽  
pp. 229-238 ◽  
Author(s):  
Kheng H. Peh ◽  
Andrew Moulson ◽  
Beatrice Y.C. Wan ◽  
El-Sayed K. Assem ◽  
Frederick L. Pearce
Keyword(s):  
Nitric Oxide ◽  
Mast Cells ◽  
Histamine Release ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
Human Basophils

Role of Nitric Oxide towards Vasodilator Effects of Substance P and ATP in Human Forearm Vessels

1997 ◽  
Vol 92 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Masanari Shiramoto ◽  
Tsutomu Imaizumi ◽  
Yoshitaka Hirooka ◽  
Toyonari Endo ◽  
Takashi Namba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Substance P ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Dependent Manner ◽  
Human Forearm ◽  
Before And After ◽  
Dose Dependent

1. It has been shown in animals that substance P as well as acetylcholine releases endothelium-derived nitric oxide and evokes vasodilatation and that ATP-induced vasodilatation is partially mediated by nitric oxide. The aim of this study was to examine whether vasodilator effects of substance P and ATP are mediated by nitric oxide in humans. 2. In healthy volunteers (n = 35), we measured forearm blood flow by a strain-gauge plethysmograph while infusing graded doses of acetylcholine, substance P, ATP or sodium nitroprusside into the brachial artery before and after infusion of NG-monomethyl-l-arginine (4 or 8 μmol/min for 5 min). In addition, we measured forearm blood flow while infusing substance P before and during infusion of l-arginine (10 mg/min, simultaneously), or before and 1 h after oral administration of indomethacin (75 mg). 3. Acetylcholine, substance P, ATP or sodium nitroprusside increased forearm blood flow in a dose-dependent manner. NG-Monomethyl-l-arginine decreased basal forearm blood flow and inhibited acetylcholine-induced vasodilatation but did not affect substance P-, ATP-, or sodium nitroprusside-induced vasodilatation. Neither supplementation of l-arginine nor pretreatment with indomethacin affected substance P-induced vasodilatation. 4. Our results suggest that, in the human forearm vessels, substance P-induced vasodilatation may not be mediated by either nitric oxide or prostaglandins and that ATP-induced vasodilatation may also not be mediated by nitric oxide.

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