scholarly journals Inhibition of the Bronchial Reaction Induced by Allergen Inhalation in Children

Respiration ◽  
1970 ◽  
Vol 27 (1) ◽  
pp. 357-357
Author(s):  
Inga Engström
2015 ◽  
Vol 46 (3) ◽  
pp. 819-831 ◽  
Author(s):  
Gail M. Gauvreau ◽  
Amani I. El-Gammal ◽  
Paul M. O'Byrne

Environmental allergens are an important cause of asthma and can contribute to loss of asthma control and exacerbations. Allergen inhalation challenge has been a useful clinical model to examine the mechanisms of allergen-induced airway responses and inflammation. Allergen bronchoconstrictor responses are the early response, which reaches a maximum within 30 min and resolves by 1–3 h, and late responses, when bronchoconstriction recurs after 3–4 h and reaches a maximum over 6–12 h. Late responses are followed by an increase in airway hyperresponsiveness. These responses occur when IgE on mast cells is cross-linked by an allergen, causing degranulation and the release of histamine, neutral proteases and chemotactic factors, and the production of newly formed mediators, such as cysteinyl leukotrienes and prostaglandin D2. Allergen-induced airway inflammation consists of an increase in airway eosinophils, basophils and, less consistently, neutrophils. These responses are mediated by the trafficking and activation of myeloid dendritic cells into the airways, probably as a result of the release of epithelial cell-derived thymic stromal lymphopoietin, and the release of pro-inflammatory cytokines from type 2 helper T-cells. Allergen inhalation challenge has also been a widely used model to study potential new therapies for asthma and has an excellent negative predictive value for this purpose.


2008 ◽  
Vol 38 (5) ◽  
pp. 829-838 ◽  
Author(s):  
G. R. Zosky ◽  
A. N. Larcombe ◽  
O. J. White ◽  
J. T. Burchell ◽  
T. Z. Janosi ◽  
...  

2018 ◽  
Vol 141 (6) ◽  
pp. 2271-2273.e7 ◽  
Author(s):  
Izumi Nishioka ◽  
Toshiro Takai ◽  
Natsuko Maruyama ◽  
Seiji Kamijo ◽  
Punyada Suchiva ◽  
...  

1995 ◽  
Vol 78 (5) ◽  
pp. 1844-1852 ◽  
Author(s):  
A. R. Berman ◽  
A. G. Togias ◽  
G. Skloot ◽  
D. Proud

Bradykinin reduces airflow in asthmatic patients via indirect mechanism(s), possibly involving sensory nerve stimulation and increased vascular permeability. We hypothesized that allergen inhalation, which affects reactivity of nerves and vessels, would differentially alter reactivity to bradykinin and the smooth muscle spasmogen methacholine. We compared reactivity to methacholine and bradykinin 1, 2, 4, 7, 11, and 14 days after allergen provocation in 12 atopic asthmatic patients with stable baseline reactivity to bradykinin. Maximal allergen-induced shifts from baseline in reactivity were 0.73 +/- 0.12 log unit for bradykinin compared with 0.27 +/- 0.13 log units for methacholine (P = 0.0005). Nine subjects showed significant increases in bradykinin reactivity, with four subjects increasing reactivity by > 1 log unit. Moreover, the maximal mean change in bradykinin reactivity occurred 2 days postallergen. Thus, allergen-induced changes in reactivity to bradykinin and methacholine differ in magnitude and time course. Bradykinin inhalational challenge provides a sensitive index of the airway's response to allergen.


Allergy ◽  
1993 ◽  
Vol 48 (3) ◽  
pp. 202-206 ◽  
Author(s):  
E. Crimi ◽  
A. Balbo ◽  
S. Voltolini ◽  
C. Troise ◽  
V. Brusasco ◽  
...  

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