Urinary leukotriene E after exercise challenge in children with asthma

Kikawa, Yoshiharu; Miyanomae, Takeshi; Inoue, Yasuhiro; Saito, Masakazu; Nakai, Asami; Shigematsu, Yousuke; Hosoi, Susumu; Sudo, Masakatsu

doi:10.1016/0091-6749(92)90294-c

Cited by 117 publications

(52 citation statements)

References 20 publications

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“…Moreover, the observations add to the similarities with EIB, as it is well established that recovery of lung function to baseline after EIB is also much faster with antagonists of the cysteinyl-LT [2,5,27,28]. Measurements of urinary LTE 4 have also demonstrated increased levels after EIB [4,5], although the magnitude is smaller and less consistent than after allergen-induced bronchoconstriction. As a technical note, it should be recognised that the time course of the bronchoconstriction after exercise and mannitol is short and this makes it very different to the prolonged airway responses that occur after allergen challenge.…”

Section: Discussionmentioning

confidence: 91%

“…Enzyme immunoassay analyses of 9a,11b-PGF 2 and LTE 4 were performed in unextracted urine samples with rabbit polyclonal antisera and acetylcholinesterase-linked tracers (Cayman Chemical Company, Ann Arbor, MI, USA) essentially as described previously [16]. However, in the present study, a different antibody was used for analysis of LTE 4 , which cross-reacted with LTE 4 to 67% and with LTC 4 and LTD 4 to 100%.…”

Section: Mediator Analysesmentioning

confidence: 99%

“…However, in the present study, a different antibody was used for analysis of LTE 4 , which cross-reacted with LTE 4 to 67% and with LTC 4 and LTD 4 to 100%. Measurement of urinary N t -methylhistamine was performed with a commercial double-antibody radioimmunoassay (Pharmacia AB, Uppsala, Sweden).…”

Section: Mediator Analysesmentioning

confidence: 99%

“…Direct evidence for mediator release following exercise in asthmatics has been obtained by an increase in the urinary levels of the mast cell marker 9a,11b-prostaglandin (PG)F 2 , a metabolite of PGD 2 , and leukotriene (LT)E 4 in association with EIB [4][5][6][7].…”

mentioning

confidence: 99%

“…To this end the urinary levels of the PGD 2 metabolite 9a,11b-PGF 2 were measured before and after a mannitol challenge in atopic asthmatics and in nonasthmatic nonatopic subjects who served as controls. The urinary excretion of N t -methylhistamine was also measured, as well as LTE 4 , in view of pharmacological data supporting the role for cysteinyl-LTs and histamine in the bronchoconstriction following the inhalation of mannitol [14].…”

mentioning

confidence: 99%

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Evidence of mast cell activation and leukotriene release after mannitol inhalation

Brannan

Gulliksson²,

Anderson³

et al. 2003

Eur Respir J

151

108

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The aim of this study was to investigate if mannitol inhalation, as a model of exercise-induced bronchoconstriction (EIB), causes mast cell activation and release of mediators of bronchoconstriction.Urinary excretion of previously identified mediators of EIB was investigated in association with mannitol-induced bronchoconstriction. Twelve asthmatic and nine nonasthmatic subjects inhaled mannitol and urine was collected 60 min before and for 90 min after challenge. The urinary concentrations of leukotriene (LT)E 4 , the prostaglandin (PG)D 2 metabolite and the mast cell marker 9a,11b-PGF 2 were measured by enzyme immunoassay. N t -methylhistamine was measured by radioimmunoassay.In asthmatic subjects, inhalation of a mean¡SEM dose of 272¡56 mg mannitol induced a reduction in forced expiratory volume in one second (FEV1) of 34.5¡2.1%. This was associated with increases in urinary 9a,11b-PGF 2 (91.9¡8.2 versus 66.9¡ 6.6 ng?mmol creatinine -1 , peak versus baseline) and LTE 4 (51.3¡7.5 versus 32.9¡4.7). In nonasthmatic subjects, the reduction in FEV1 was 1.0¡0.5% after inhaling 635 mg of mannitol. Although smaller than in the asthmatics, significant increases of urinary 9a,11b-PGF 2 (68.4¡6.9 versus 56.0¡5.8 ng?mmol creatinine -1 ) and LTE 4 (58.5¡5.3 versus 43.0¡3.3 ng?mmol creatinine -1 ) were observed in the nonasthmatic subjects. There was also a small increase in urinary excretion of N t -methylhistamine in the nonasthmatics, but not in the asthmatics.The increased urinary levels of 9a,11b-prostaglandin F 2 support mast cell activation with release of mediators following inhalation of mannitol. Increased bronchial responsiveness to the released mediators could explain the exclusive bronchoconstriction in asthmatic subjects. Eur Respir J 2003; 22: 491-496.

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