Further characterisation of substance P induced histamine release from human bronchoalveolar lavage mast cells

1996 ◽  
Vol 45 (S1) ◽  
pp. S11-S12 ◽  
Author(s):  
L. J. M. Cross ◽  
L. G. Heaney ◽  
M. Ennis
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Bronchoalveolar Lavage ◽  
Histamine Release

Release of Histamine from Dural Mast Cells by Substance P and Calcitonin Gene-Related Peptide

Cephalalgia ◽  
1997 ◽  
Vol 17 (3) ◽  
pp. 166-174 ◽  
Author(s):  
A Ottosson ◽  
L Edvinsson
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Histamine Release ◽  
Dura Mater ◽  
Neurogenic Inflammation ◽  
Calcitonin Gene Related Peptide ◽  
Sampling Procedure ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Peritoneal Mast Cells

The aim of the present study was to examine if the neuropeptides substance P (SP), calcitonin gene-related peptide (CGRP), neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) can stimulate histamine release from mast cells in the dura mater and thereby play a role in cranial vasoregulation and local neurogenic inflammation. Dura mater mast cells were compared with peritoneal mast cells in the rat. Histamine was released from dura mater mast cells by compound 48/80, SP and CGRP but from peritoneal mast cells only by compound 8/80 and SP. NPY and VIP released quite small amounts of histamine from dural mast cells. The release on SP and CGRP from rat dura mater mast cells was blocked by the receptor antagonists FK888 and CGRP8-37 respectively, suggesting receptor mediated release mechanisms. None of the stimuli released histamine from human or porcine dural mast cells, possibly because the sampling procedure injures and incapacitates the cells.

Substance P-induced histamine release in tracheally perfused guinea pig lungs

1995 ◽  
Vol 78 (4) ◽  
pp. 1234-1241 ◽  
Author(s):  
C. M. Lilly ◽  
A. E. Hall ◽  
I. W. Rodger ◽  
L. Kobzik ◽  
K. J. Haley ◽  
...  
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Guinea Pig ◽  
Histamine Release ◽  
Receptor Activation ◽  
Neurokinin A ◽  
Histamine Liberation ◽  
Nk1 Antagonist ◽  
Nk2 Receptor ◽  
Receptor Agonists And Antagonists

The capacity of substance P (SP) and endogenously released tachykinins to liberate histamine was examined in isolated tracheally perfused guinea pig lungs. Increasing doses of tracheally injected SP were associated with the recovery of increasing amounts of histamine from lung effluent. The mechanism of SP-induced histamine liberation was explored in studies with neurokinin-(NK) receptor agonists and antagonists. Tracheal injection of either the NK1 agonist [Sar9,Met(O2)11]SP or the NK2 agonist [beta-Ala8]-neurokinin A-(4–10) was associated with a significant increase in histamine recovery from lung effluent. In addition, both the NK1 antagonist CP-99994 and the NK2 antagonist SR-48968 significantly inhibited SP-induced histamine release. These findings support the hypothesis that SP can liberate histamine from guinea pigs lungs by a mechanism that depends predominantly on NK1- and NK2-receptor activation. The liberation of endogenous tachykinins by acute tracheal injection of capsaicin was also associated with augmented histamine recovery, which was inhibited by combined NK1- and NK2-receptor blockade. Tracheal injection of SP was associated with an increase in the percentage of airway mast cells exhibiting histological evidence of degranulation. This study demonstrates that exogenous SP, as well as endogenous tachykinins released from capsaicin-sensitive neurons, can liberate histamine, most likely from airway mast cells, by a mechanism that depends predominantly on the activation of NK1 and NK2 receptors.

Regulation of histamine release from human bronchoalveolar lavage mast cells by stem cell factor in several respiratory diseases

Allergy ◽  
1995 ◽  
Vol 50 (4) ◽  
pp. 340-348 ◽  
Author(s):  
R. Louis ◽  
P. Tilkin ◽  
M. Poncelet ◽  
J. L Corhay ◽  
P. Mendez ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mast Cells ◽  
Bronchoalveolar Lavage ◽  
Histamine Release ◽  
Stem Cell Factor ◽  
Respiratory Diseases

Adenosine induces histamine release from human bronchoalveolar lavage mast cells

1999 ◽  
Vol 96 (4) ◽  
pp. 349-355 ◽  
Author(s):  
P. FORSYTHE ◽  
L. P. A. MCGARVEY ◽  
L. G. HEANEY ◽  
J. MACMAHON ◽  
M. ENNIS
Keyword(s):  
Mast Cells ◽  
Bronchoalveolar Lavage ◽  
Histamine Release ◽  
Adenosine Receptor ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Maximal Response ◽  
Adenosine Receptor Agonists ◽  
Receptor Agonists ◽  
Endogenous Adenosine

Previous studies have shown that in vitroadenosine enhances histamine release from activated human lung mast cells obtained by enzymic dispersion of lung parenchyma. However, adenosine alone has no effect on histamine release from these cells. Given the evidence for direct activation of mast cells after endobronchial challenge with adenosine and previous studies indicating that mast cells obtained at bronchoalveolar lavage are a better model for asthma studies than those obtained by enzymic dispersion of lung tissue, the histamine-releasing effect of adenosine was examined on lavage mast cells. Bronchoalveolar lavage fluid was obtained from patients attending hospital for routine bronchoscopy (n = 54). Lavage cells were challenged with adenosine or adenosine receptor agonists (20 min, 37 °C) and histamine release determined using an automated fluorometric assay. Endogenous adenosine levels were also measured in lavage fluid (n = 9) via an HPLC method. Adenosine alone caused histamine release from lavage mast cells in 37 of 54 patients with a maximal histamine release of 20.56±2.52% (range 5.2–61%). The adenosine receptor agonists (R)-N6-(2-phenylisopropyl)adenosine, 5'-N-ethylcarboxamidoadenosine and CGS21680 also induced histamine release from lavage mast cells. Preincubation of lavage mast cells with the adenosine receptor antagonist xanthine amine congener caused significant inhibition of the response to adenosine (P = 0.007). There was an inverse correlation between endogenous adenosine levels in the lavage fluid and the maximal response to in vitro adenosine challenge of the lavage cells. The findings of the present study indicate a means by which adenosine challenge of the airways can induce bronchoconstriction and support a role for adenosine in the pathophysiology of asthma. The results also suggest that cells obtained from bronchoalveolar lavage fluid may provide the ideal model for the testing of novel, adenosine receptor, targeted therapies for asthma.

Substance P induces histamine release from human pulmonary mast cells

1995 ◽  
Vol 25 (2) ◽  
pp. 179-186 ◽  
Author(s):  
L. G. HEANEY ◽  
L. J. M. CROSS ◽  
C. F. STANFORD ◽  
M. ENNIS
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Histamine Release
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