Targeted eicosanoid lipidomics of exhaled breath condensate provide a distinct pattern in the aspirin-intolerant asthma phenotype

Sanak, Marek; Gielicz, Anna; Bochenek, Grażyna; Kaszuba, Marek; Niżankowska‐Mogilnicka, Ewa; Szczeklik, A

doi:10.1016/j.jaci.2010.12.1108

Cited by 65 publications

(52 citation statements)

References 38 publications

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“…The studied AIA subgroup was also characterized by increased baseline concentration of CysLTs and LTC 4 in EBC. It is consistent with earlier study using immunoassay [2], although other studies using spectrometric methods did not demonstrate baseline overproduction of CysLTs [22] or LTC 4 [24] in the airways in AIA. However, our observation is in line with researches assessing LTC 4 level in induced sputum [18] and can be related to overexpression of LTC synthase (LTCS) in eosinophils [23] and bronchi [21] of asthmatics with aspirin hypersensitivity.…”

Section: Discussionsupporting

confidence: 92%

“…Concentration of eicosanoids in exhaled breath condensate was measured using gas chromatography/mass spectrometry (GC-MS) and high-performance liquid chromatography/ tandem mass spectrometry (HPLC-MS/MS) according to the methodology described elsewhere [24,25]. The results were reported in picograms per milliliter of EBC (pg/ml), or recalculated as picograms per microgram of palmitic acid content (pg/μg of PA) due to variable dilution by condensed water.…”

Section: Biochemical Assaysmentioning

confidence: 99%

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Eicosanoids in exhaled air after non-specific challenge in patients with asthma

Kaszuba¹,

Kaszuba²,

Sawina³

et al. 2013

Hypersensitivity

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Background: Histamine is used as a direct stimulus to measure airway responsiveness. This short-acting biogenic amine acts mainly on airway smooth muscle receptors causing bronchoconstriction and is used for the airway hyperresponsiveness assessment in asthmatic patients. In aspirin-induced asthma (AIA) special regulatory role of eicosanoids is postulated. The aim of the study was to assess the influence of histamine on a wide profile of eicosanoids measured in exhaled breath condensate (EBC) in AIA patients and asthmatics tolerating aspirin well (ATA). Methods:The study population consisted of seventeen asthmatics. Ten of them were AIA patients. Eicosanoid concentrations in EBC were determined using gas chromatography/mass spectrometry or high-performance liquid chromatography/tandem mass spectrometry. Measurements were performed at baseline and following bronchial histamine challenge. Results: Bronchial reactions were precipitated by histamine in all patients and accompanied only by decrease of leukotriene (LT) C 4 and trans-LTC 4 mean level. The AIA group was characterized by higher levels of cysteinyl leukotrienes, LTC 4 , and prostaglandin (PG) E 2 in EBC at baseline, and decrease in EBC concentration of LTC 4 , trans-LTC 4 and tetranor-PGE-M following histamine challenge. In the ATA group no significant changes in eicosanoids levels after histamine were noticed. Conclusions: AIA patients present different baseline profile of EBC eicosanoids in comparison to patients with ATA. Histamine administered locally during a bronchial challenge test may influence inflammatory mediators and thus trigger indirect effects in the respiratory tract. This response for histamine differentiates two studied phenotypes of asthma; only in the AIA group histamine precipitates alterations of the eicosanoid synthesis in the lungs. Keywords: Aspirin, asthma, hypersensitivity, eicosanoids, histamine © 2013 Kaszuba et al; licensee Herbert Publications Ltd. This is an Open Access article distributed under the terms of Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0). This permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. IntroductionHistamine is a short-acting biogenic amine which plays an important role in allergic inflammation. Mast cells and basophiles store large quantities of histamine, which is released during degranulation in response to immunologic and nonimmunologic stimuli [1]. Histamine elicits many biological effects acting through four types of histamine receptors located on cells of various types. These include airway smooth muscle cells provoking airflow obstruction and sensory fibers causing a reflex response that can induce bronchospasm. Histamine, beside methacholine, is used as a direct stimulus to measure airway responsiveness.Airway hyperresponsiveness (AHR) is one of the clinical features of asthma. Its measurement is crucial for establishing the correct diagnosis [17]. The components of airway changes in...

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Section: Discussionsupporting

confidence: 92%

Section: Biochemical Assaysmentioning

confidence: 99%

Eicosanoids in exhaled air after non-specific challenge in patients with asthma

Kaszuba¹,

Kaszuba²,

Sawina³

et al. 2013

Hypersensitivity

Self Cite

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“…Eoxins are known as 15-LOX analogues of cysLTs, and their biological properties regarding the permeability-increasing activity are similar [28]. It is suggested that eoxin overproduction may be involved in the pathogenesis of AERD [28]; however, high eoxin levels are not consistently reported in AERD [34,35]. This is the first study to report that identified serum eoxin C 4 metabolite levels are higher in patients with AERD than in patients with ATA and increased significantly during the Lys-ASA BPT in patients with AERD.…”

Section: Discussionmentioning

confidence: 99%

Metabolomic analysis identifies potential diagnostic biomarkers for aspirin‐exacerbated respiratory disease

Ban

Cho

Kim

et al. 2016

Clin Experimental Allergy

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SummaryBackground To date, there has been no reliable in vitro test to diagnose aspirin-exacerbated respiratory disease (AERD). Objective To investigate potential diagnostic biomarkers for AERD using metabolomic analysis. Methods An untargeted profile of serum from asthmatics in the first cohort (group 1) comprising 45 AERD, 44 patients with aspirin-tolerant asthma (ATA), and 28 normal controls was developed using the ultra-high-performance liquid chromatography (UHPLC)/QToF MS system. Metabolites that discriminate AERD from ATA were quantified in both serum and urine, which were collected before (baseline) and after the lysine-aspirin bronchoprovocation test (Lys-ASA BPT). The serum metabolites were validated in the second cohort (group 2) comprising 50 patients with AERD and 50 patients with ATA. Results A clear discrimination of metabolomes was found between patients with AERD and ATA. In group 1, serum levels of LTE 4 and LTE 4 /PGF 2 a ratio before and after the Lys-ASA BPT were significantly higher in patients with AERD than in patients with ATA (P < 0.05 for each), and urine baseline levels of these two metabolites were significantly higher in patients with AERD. Significant differences of serum metabolite levels between patients with AERD and ATA were replicated in group 2 (P < 0.05 for each). Moreover, serum baseline levels of LTE 4 and LTE 4 /PGF 2 a ratio discriminated AERD from ATA with 70.5%/71.6% sensitivity and 41.5%/62.8% specificity, respectively (AUC = 0.649 and 0.732, respectively P < 0.001 for each). Urine baseline LTE 4 levels were significantly correlated with the fall in FEV 1 % after the Lys-ASA BPT in patients with AERD (P = 0.008, r = 0.463). Conclusions and Clinical Relevance Serum metabolite level of LTE 4 and LTE 4 /PGF 2 a ratio was identified as potential in vitro diagnostic biomarkers for AERD using the UHPLC/QToF MS system, which were closely associated with major pathogenetic mechanisms underlying AERD.

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“…The eicosanoids that were found to be elevated baseline in aspirin sensitive patients were 5 and 15-hydroxyeicosatetraenoic acid (HETE). Another study reported significant increase in the level ofprostaglandin D2 and E2 metabolites and 5-, 15-HETE in aspirin intolerant asthma patients by usingcomplementary high performance liquid chromatography (HPLC) and gas chromatography-massspectrometry (GC/MS) [52]. The authors proposed that highly sensitive eicosanoid profiling in EBC can be used to identify aspirin intolerant asthma phenotypes.…”

Section: Lipid Mediatorsmentioning

confidence: 99%

Exhaled Breath Condensates as a Source for Biomarkers for Characterization of Inflammatory Lung Diseases

Bajaj¹,

Ishmael²

2013

JASMI

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Inflammatory lung diseases such as asthma and chronic obstructive pulmonary disease are common and difficult to diagnose and characterize. This is due in large part to difficulty in obtaining samples directly from the inflamed lung. The collection of lung secretions by traditional methods including bronchoalveolar lavage and induced sputum collection are limited by their invasive nature. Exhaled breath condensate (EBC) is a simple and non-invasive technique of collecting fluid samples, which are representative of airway lining fluid. Advances in collection methods and evolving molecular techniques have led to development of more sensitive assays for existing biomarkers and identification of new biomarkers, which can be potentially useful in monitoring lung inflammation. In this review, we present the current understanding of various biomarkers including small molecules (H 2 O 2 , pH and nitric oxide related biomarkers), lipid mediators (8-isprostane, leukotrienes and prostaglandins), small proteins (cytokines and chemokines) and nucleic acids (DNA and microRNAs). We also discuss the differential profile of biomarkers in recognizing different patterns of lung inflammation. As the sensitivity of methods of EBC improves, this biofluid will play an increasing role in diagnosis and monitoring of lung diseases.

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Targeted eicosanoid lipidomics of exhaled breath condensate provide a distinct pattern in the aspirin-intolerant asthma phenotype

Cited by 65 publications

References 38 publications

Eicosanoids in exhaled air after non-specific challenge in patients with asthma

Eicosanoids in exhaled air after non-specific challenge in patients with asthma

Metabolomic analysis identifies potential diagnostic biomarkers for aspirin‐exacerbated respiratory disease

Exhaled Breath Condensates as a Source for Biomarkers for Characterization of Inflammatory Lung Diseases

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