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

Stenberg, Henning ; Wadelius, Erik ; Moitra, Subhabrata ; Åberg, Ida LU ; Ankerst, Jaro LU orcid ; Diamant, Zuzana LU ; Bjermer, Leif LU and Tufvesson, Ellen LU (2018) In Biomarkers 23(1). p.51-60
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.... (More)

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.

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author
; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
airway epithelium, Asthma, bronchoalveolar lavage, club cell protein (CC16), inhaled allergen challenge, mannitol challenge
in
Biomarkers
volume
23
issue
1
pages
51 - 60
publisher
Taylor & Francis
external identifiers
  • pmid:28862880
  • scopus:85029572208
ISSN
1354-750X
DOI
10.1080/1354750X.2017.1375559
language
English
LU publication?
yes
id
060a14ba-5418-40c2-adcb-344537c75b4f
date added to LUP
2017-09-29 10:52:45
date last changed
2024-03-31 17:32:49
@article{060a14ba-5418-40c2-adcb-344537c75b4f,
  abstract     = {{<p>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.</p>}},
  author       = {{Stenberg, Henning and Wadelius, Erik and Moitra, Subhabrata and Åberg, Ida and Ankerst, Jaro and Diamant, Zuzana and Bjermer, Leif and Tufvesson, Ellen}},
  issn         = {{1354-750X}},
  keywords     = {{airway epithelium; Asthma; bronchoalveolar lavage; club cell protein (CC16); inhaled allergen challenge; mannitol challenge}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{51--60}},
  publisher    = {{Taylor & Francis}},
  series       = {{Biomarkers}},
  title        = {{Club cell protein (CC16) in plasma, bronchial brushes, BAL and urine following an inhaled allergen challenge in allergic asthmatics}},
  url          = {{http://dx.doi.org/10.1080/1354750X.2017.1375559}},
  doi          = {{10.1080/1354750X.2017.1375559}},
  volume       = {{23}},
  year         = {{2018}},
}