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变应性哮喘患者吸入变应原激发后血浆、支气管刷检物、支气管肺泡灌洗液及尿液中的克拉拉细胞蛋白(CC16)

Club cell protein (CC16) in plasma, bronchial brushes, BAL and urine following an inhaled allergen challenge in allergic asthmatics.

作者信息

Stenberg Henning, Wadelius Erik, Moitra Subhabrata, Åberg Ida, Ankerst Jaro, Diamant Zuzana, Bjermer Leif, Tufvesson Ellen

机构信息

a Department of Clinical Sciences, Respiratory Medicine and Allergology , Lund University , Lund , Sweden.

b Department of Clinical Pharmacy and Pharmacology, and QPS-NL , University Medical Center Groningen , Groningen , The Netherlands.

出版信息

Biomarkers. 2018 Feb;23(1):51-60. doi: 10.1080/1354750X.2017.1375559. Epub 2017 Sep 18.

DOI:10.1080/1354750X.2017.1375559
PMID:28862880
Abstract

BACKGROUND

Club cell protein (CC16) is a pneumoprotein secreted by epithelial club cells. CC16 possesses anti-inflammatory properties and is a potential biomarker for airway epithelial damage. We studied the effect of inhaled allergen on pulmonary and systemic CC16 levels.

METHODS

Thirty-four subjects with allergic asthma underwent an inhaled allergen challenge. Bronchoscopy with bronchoalveolar lavage (BAL) and brushings was performed before and 24 h after the challenge. CC16 was quantified in BAL and CC16 positive cells and CC16 mRNA in bronchial brushings. CC16 was measured in plasma and urine before and repeatedly after the challenge. Thirty subjects performed a mannitol inhalation challenge prior to the allergen challenge.

RESULTS

Compared to baseline, CC16 in plasma was significantly increased in all subjects 0-1 h after the allergen challenge, while CC16 in BAL was only increased in subjects without a late allergic response. Levels of CC16 in plasma and in the alveolar fraction of BAL correlated significantly after the challenge. There was no increase in urinary levels of CC16 post-challenge. Mannitol responsiveness was greater in subjects with lower baseline levels of CC16 in plasma.

CONCLUSIONS

The increase in plasma CC16 following inhaled allergen supports the notion of CC16 as a biomarker of epithelial dysfunction.

摘要

背景

克拉拉细胞蛋白(CC16)是一种由上皮克拉拉细胞分泌的肺蛋白。CC16具有抗炎特性,是气道上皮损伤的潜在生物标志物。我们研究了吸入变应原对肺部和全身CC16水平的影响。

方法

34名过敏性哮喘患者接受了吸入变应原激发试验。在激发试验前和激发后24小时进行支气管镜检查及支气管肺泡灌洗(BAL)和刷检。对BAL中的CC16进行定量分析,并检测支气管刷检中的CC16阳性细胞和CC16 mRNA。在激发试验前及激发后多次检测血浆和尿液中的CC16。30名受试者在变应原激发试验前进行了甘露醇吸入激发试验。

结果

与基线相比,变应原激发试验后0 - 1小时所有受试者血浆中的CC16均显著升高,而只有无迟发性过敏反应的受试者BAL中的CC16升高。激发试验后血浆和BAL肺泡部分的CC16水平显著相关。激发试验后尿液中CC16水平没有升高。血浆中CC16基线水平较低的受试者对甘露醇的反应性更高。

结论

吸入变应原后血浆CC16升高支持了CC16作为上皮功能障碍生物标志物的观点。

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