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In vivo restitution of airway epithelium
TLDR
It is concluded that reproducible shedding-like denudation, without bleeding or damage to the basement membrane, can be produced in vivo and rapid restitution of airway epithelium may depend on contributions from the microcirculation and innervation.
Natural Killer Cells Determine Development of Allergen-induced Eosinophilic Airway Inflammation in Mice
TLDR
It is demonstrated that depletion of NK1.1+ cells before immunization inhibits pulmonary eosinophil and CD3+ T cell infiltration as well as increased levels of interleukin (IL)-4, IL-5, and IL-12 in bronchoalveolar lavage fluid in a murine model of allergic asthma, suggesting a critical role of NK cells, but not of NKT cells, for the development of allergen-induced airway inflammation.
Allergic Eosinophil-rich Inflammation Develops in Lungs and Airways of B Cell–deficient Mice
TLDR
Immunization to OVA followed by OVA challenges thus cause eosinophil-rich inflammation in airways and lungs of mice without involvement of B cells and Ig, and this paradigm is validated in homozygous mutant C57BL/6 mice.
Effects of bronchoconstrictors and bronchodilators on a novel human small airway preparation
TLDR
Theophylline and enprofylline consistently relaxed the bronchiolar preparations including those exhibiting little responsiveness to the β2‐adrenoceptor agonist, suggesting antagonism of adenosine receptors is probably not involved in relaxation of the small airways.
Capsaicin-induced cough in humans.
TLDR
Capsaicin-induced cough is characterized and it is demonstrated that it can be a useful tool in the study of cough reactivity and for evaluation of antitussive agents in humans.
Effects of prostaglandins on the isolated human bladder and urethra.
TLDR
Urethral preparations contracted by PGF2 alpha or noradrenaline were relaxed by these agents; this relaxing effect was at least as pronounced as that produced by isoprenaline; it was not affected by propranolol.
Antagonism of the prostaglandin D2 receptor CRTH2 attenuates asthma pathology in mouse eosinophilic airway inflammation
TLDR
The data suggest that CRTH2 antagonism alone is effective in mouse allergic airway inflammation even to the extent that this mechanism can explain the efficacy of ramatroban.
Allergen-induced eosinophil cytolysis is a primary mechanism for granule protein release in human upper airways.
TLDR
The nature and extent of the ECL and its product indicate that allergen-induced cytolysis is a primary and major mechanism for the release of eosinophil proteins in human allergic airway inflammation in vivo.
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