Absence of a late-phase response or increase in histamine responsiveness after bronchial provocation with adenosine 5′-monophosphate in atopic and non-atopic asthma

1988 ◽  
Vol 75 (4) ◽  
pp. 429-436 ◽  
Author(s):  
G. D. Phillips ◽  
S. T. Holgate
Keyword(s):  
Mast Cell ◽  
Late Phase ◽  
Forced Expiratory Volume ◽  
Atopic Asthma ◽  
Phase Reaction ◽  
Bronchial Responsiveness ◽  
Late Phase Reaction ◽  
Inflammatory Changes ◽  
Bronchial Provocation ◽  
Airway Calibre

1. Adenosine 5′-monophosphate (AMP) causes bronchoconstriction in atopic and non-atopic asthma by a mechanism believed to involve histamine release from airway mast cells. To determine whether preformed mast cell mediators, principally histamine, can initiate a late-phase bronchoconstriction we have investigated the effect on the airways over a 24 h period of a single bronchial challenge with AMP. 2. Six atopic asthmatic subjects (all late responders to inhaled allergen) and six non-atopic asthmatic subjects were studied on two occasions for a 24 h period after inhalation of the provocation concentration of AMP required to produce a 20% fall in forced expiratory volume in 1 s (FEV1) from baseline (PC20) and 0.9% (w/v) sodium chloride placebo, respectively. The atopic asthmatic subjects were studied on a further occasion after challenge with the PC20 allergen. 3. Inhalation of the PC20 AMP resulted in an immediate fall in FEV1 to a mean maximum 25.5% below baseline without resulting in any late decrease in airway calibre. No significant increase in non-specific bronchial responsiveness as determined by measuring the PC20 histamine before, and at 3, 9 and 24 h after, AMP challenge, occurred. Inhalation of the PC20 allergen caused a reproducible late-phase bronchoconstriction and increase in non-specific bronchial responsiveness in all the atopic asthmatic subjects studied. 4. These results suggest that preformed mast cell mediators, principally histamine, play no role in the initiation of the late-phase reaction in allergen-provoked asthma, although they may contribute to the inflammatory changes involved.

Rapid reversibility of the allergen-induced pulmonary late-phase reaction by an intravenous β2-agonist

1998 ◽  
Vol 84 (5) ◽  
pp. 1500-1505 ◽  
Author(s):  
R. Stokes Peebles ◽  
Solbert Permutt ◽  
Alkis Togias
Keyword(s):  
Lung Function ◽  
Vital Capacity ◽  
Late Phase ◽  
Allergen Challenge ◽  
Forced Expiratory Volume ◽  
Phase Reaction ◽  
Phase Reduction ◽  
Late Phase Reaction ◽  
Kinetics Of ◽  
Β2 Agonist

This study was performed to determine the degree to which β2-adrenergic receptor agonists can reverse the allergen-induced late reduction in lung function. On two occasions, seven asthmatic subjects were administered terbutaline or its vehicle by intravenous infusion 7 h after inhaled allergen, at which point the forced expiratory volume in 1 s was 57% of baseline. On another occasion, terbutaline was infused at baseline to determine maximal attainable bronchodilation. After allergen challenge, terbutaline rapidly improved lung function. At the end of terbutaline infusion, the forced expiratory volume in 1 s reached 100 ± 1.3% of baseline and 84.2 ± 4.3% of maximal attainable value, but the bronchodilating effect of the β-agonist did not plateau. The values for forced vital capacity were 102 ± 1.3% of baseline and 95.1 ± 3% of maximal attainable value. The kinetics of the terbutaline effect, when it was infused at baseline, were similar to those in the late phase. Because the late-phase reduction in lung function is rapidly reversible by β2-adrenergic agonists, we conclude that it is caused mainly by bronchial smooth muscle spasm.

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.

Development of eosinophilic conjunctival inflammation at late-phase reaction in mast cell–deficient mice

2007 ◽  
Vol 120 (2) ◽  
pp. 476-478 ◽  
Author(s):  
Mayumi Ueta ◽  
Takao Nakamura ◽  
Satoshi Tanaka ◽  
Kentaro Kojima ◽  
Shigeru Kinoshita
Keyword(s):  
Mast Cell ◽  
Late Phase ◽  
Phase Reaction ◽  
Late Phase Reaction ◽  
Conjunctival Inflammation ◽  
Deficient Mice

Lack of interaction of hyperpnoea with methacholine and histamine in asthma

1998 ◽  
Vol 95 (5) ◽  
pp. 611-619 ◽  
Author(s):  
Suree SOMPRADEEKUL ◽  
Rana HEJAL ◽  
Melissa McLANE ◽  
K. A. LENNER ◽  
J. A. NELSON ◽  
...  
Keyword(s):  
Blood Flow ◽  
Forced Expiratory Volume ◽  
Additive Effects ◽  
Positive Interaction ◽  
Bronchial Responsiveness ◽  
Individual Effects ◽  
The Individual ◽  
Airway Calibre ◽  
Effector Mechanisms

1.The thermal precipitants of asthma (exercise and hyperventilation) appear to have a unique pathogenesis that does not alter bronchial responsiveness. In the present work, we tested whether hyperpnoea interacts with other constrictor stimuli. 2.To provide data on this issue, we exposed 17 subjects with asthma to isocapnic hyperventilation of frigid air (HV), methacholine (METH) and histamine (HIS) alone and in combination. 3.With HV (mean ventilation = 55.6±7.7 litres/min), METH (2.20±0.7 ;mmol/l) and HIS (10.35±5.04 ;mmol/l) alone, the decrements in forced expiratory volume in 1 ;s (FEV1) from baseline were 27.4±3.4, 27.4±3.8 and 32.4±3% respectively (n = 9). Giving the agonists simultaneously did not produce additive effects (ΔFEV1 HV+METH = 32.8±3.6%; HV+HIS = 28.7±5.1%). None of the individual or combined responses was significantly different from each other. Changing the sequence of the experiments and giving METH at the height of the HV-induced bronchial narrowing, instead of during hyperpnoea, did not alter the findings (n = 8). The maximum fall in FEV1 after both bronchoconstrictors in this experiment (ΔFEV1 = 32.3±4.3%) was not significantly different from either alone (HV = 22.8±1.0%; METH = 27.3±1.9%). When METH and HIS were administered together, however (n = 5), a positive interaction ensued (METH = 1.53±0.56 ;mmol/l, ΔFEV1 = 15.6±4.6%; HIS = 4.77±2.07 ;mmol/l, ΔFEV1 = 18.8±3.1%; METH+HIS ΔFEV1 = 33.4±5.2%; P< 0.001 compared with the individual effects). 4.These results indicate that HV does not interact with stimuli that directly or indirectly modulate airway calibre. It is unclear if this effect represents protection conferred from increased bronchial blood flow or derives from differences in effector mechanisms between the thermal and pharmacological agonists.

Childhood Asthma: Overview

1989 ◽  
Vol 10 (8) ◽  
pp. 227-233
Author(s):  
M. J. Goldenhersh ◽  
Gary S. Rachelefsky
Keyword(s):  
Childhood Asthma ◽  
Chronic Cough ◽  
Late Phase ◽  
Inflammatory Cells ◽  
Polymorphonuclear Cells ◽  
Phase Reaction ◽  
Recurrent Pneumonia ◽  
Late Phase Reaction ◽  
Airway Response ◽  
Trachea And Bronchi

DEFINITION Asthma is a syndrome characterized by increased responsiveness of the trachea and bronchi to various stimuli and is manifested by widespread reversible narrowing of the airways that changes in severity either spontaneously or as a result of therapy.1 The hyperresponsiveness ("twitchiness") of airways is a fundamental abnormality and is dynamic in nature. Asthma is a disease of persistent or recurrent airway inflammation characterized by the presence of inflammatory cells (eosinophils and polymorphonuclear cells), edema of the wall, and changes in epithelial cells. Airway response to allergens and certain irritants may be acute (occurring within minutes to one hour following exposure), delayed or late (occurring within four to eight hours following exposure), or dual (combination of acute and late phase). Some reactions are only delayed. The late phase reaction is largely attributed to ongoing inflammation. Because of the variability of its presentation (complete v partial reversibility of airways obstruction, hyperreactivity accompanying other respiratory disease, chronic cough, or recurrent pneumonia with or without wheeze), children have often been denied appropriate antiasthmatic medications and their symptoms have been attributed instead to "wheezy bronchitis," "recurrent bronchiolitis," "spastic bronchitis," or "wheezy baby syndrome." For years pediatricians have been schooled to approach the wheezing child skeptically ("all that wheezes is not asthma").

scholarly journals IL-9+ IL-10+ T cells link immediate allergic response to late phase reaction

2011 ◽  
Vol 165 (1) ◽  
pp. 29-37 ◽  
Author(s):  
S.-H. He ◽  
Z.-Q. Liu ◽  
X. Chen ◽  
C.-H. Song ◽  
L.-F. Zhou ◽  
...  
Keyword(s):  
T Cells ◽  
Late Phase ◽  
Allergic Response ◽  
Phase Reaction ◽  
Late Phase Reaction
Sign in / Sign up

Export Citation Format

Share Document