Increase in inflammatory mediator concentrations in exhaled breath condensate after allergen inhalation.
BACKGROUND
Although a number of studies have been carried out to examine the baseline concentrations of inflammatory mediators in asthmatic patients, the clinical utility of exhaled breath condensate (EBC) in allergen-induced bronchoconstriction has not yet been clarified.


OBJECTIVE
We examined whether the release of inflammatory mediators can be detected in EBC after allergen-induced bronchoconstriction in asthmatic patients.


METHODS
We quantified mast cell-associated mediators in EBC and their corresponding urinary metabolites before and after allergen inhalation.


RESULTS
Early asthmatic responses (EARs) caused significant increases in the concentrations of cysteinyl leukotrienes (CysLTs; median, 10.4 vs 99.0 pg/mL; P < .0001) and prostaglandin D(2) (PGD(2); median, 2.26 vs 8.72 pg/mL; P = .0077), but not that of histamine, from baseline concentrations. Significant increases in the concentrations of urinary leukotriene E(4) and 9alpha, 11beta-prostaglandin F(2) were detected in patients with EARs. However, the percentage increases in the concentrations of CysLTs and PGD(2) in EBC did not correlate with those of their corresponding urinary metabolites. The increases in concentrations of CysLTs and PGD(2) in EBC in patients with EARs correlated with each other and correlated with the extent of decrease in FEV(1). An insignificant difference in tyrosine concentration before and after the inhalation test demonstrated that errors caused by dilution of inflammatory mediators are negligibly small in EBC collected over a short period.


CONCLUSIONS
In patients with allergen-induced EARs, pulmonary generation of mast cell-associated mediators can be evaluated by quantifying CysLTs and PGD(2) in EBC, suggesting that the quantification of EBC mediators might be useful in monitoring acute asthmatic airway inflammation.
Ono
Emiko
E
Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan; Division of the Third Department of Internal Medicine, Oita University School of Medicine, Yuhu, Oita, Japan. Electronic address: e-ono@sagamihara-hosp.gr.jp.
Mita
Haruhisa
H
Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan.
Taniguchi
Masami
M
Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan.
Higashi
Noritaka
N
Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan.
Tsuburai
Takahiro
T
Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan.
Hasegawa
Maki
M
Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan.
Miyazaki
Eishi
E
Division of the Third Department of Internal Medicine, Oita University School of Medicine, Yuhu, Oita, Japan.
Kumamoto
Toshihide
T
Division of the Third Department of Internal Medicine, Oita University School of Medicine, Yuhu, Oita, Japan.
Akiyama
Kazuo
K
Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Sagamihara, Kanagawa, Japan.
D000280:Administration, Inhalation; D000293:Adolescent; D000328:Adult; D000485:Allergens / Q000008:administration & dosage*; D001249:Asthma / Q000378:metabolism*; D016084:Bronchoconstriction / Q000187:drug effects*; D045853:Exhalation; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis / Q000378:metabolism*; D008297:Male; D008407:Mast Cells / Q000378:metabolism; D008875:Middle Aged; D008991:Monitoring, Physiologic / Q000379:methods; D012129:Respiratory Function Tests / Q000379:methods
D000485:Allergens; D018836:Inflammation Mediators