ArticlePloS one2016
Increased Expression of CC16 in Patients with Idiopathic Pulmonary Fibrosis.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 52 citations in OpenAlex.
- Pulmonary fibrosis after COVID-19 is characterized by airway abnormalities and elevated club cell secretory protein-16.JCI insight · 2026Article
- Serum vesicle biomarkers reflect the disease activity of idiopathic pulmonary fibrosis.Journal of translational medicine · 2025Article
- Mechanisms on How Matricellular Microenvironments Sustain Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2025Review
- Advances in idiopathic pulmonary fibrosis diagnosis and treatment.Chinese medical journal pulmonary and critical care medicine · 2025Review
- Nomogram model using serum Club cell secretory protein 16 to predict prognosis and acute exacerbation in patients with idiopathic pulmonary fibrosis.European journal of medical research · 2025Article
- Review
- Berberine protects against lung injury induced by liver transplantation through upregulating PPARγ and suppressing NF-κB-mediated pyroptosis pathway.Acta cirurgica brasileira · 2025Article
- Clara cell 16 kDa protein: an important marker for COVID-19 severity.Frontiers in immunology · 2025Article
- SCGB1A1 as a Key Regulator of Splenic Immune Dysfunction in COPD: Insights From a Murine Model.International journal of chronic obstructive pulmonary disease · 2025Article
- Controlled human exposures: a review and comparison of the health effects of diesel exhaust and wood smoke.Particle and fibre toxicology · 2024Review
- The multiple facets of the club cell in the pulmonary epithelium.Histology and histopathology · 2024Review
- Club Cells-A Guardian against Occupational Hazards.Biomedicines · 2023Review
- Exploring the Role of Biomarkers Associated with Alveolar Damage and Dysfunction in Idiopathic Pulmonary Fibrosis-A Systematic Review.Journal of personalized medicine · 2023Review
- Predicting Lung Function Using Biomarkers in Alpha-1 Antitrypsin Deficiency.Biomedicines · 2023Article
- Cellular and molecular features of COVID-19 associated ARDS: therapeutic relevance.Journal of inflammation (London, England) · 2023Review
- Diagnosis of Fibrotic Hypersensitivity Pneumonitis: Is There a Role for Biomarkers?Life (Basel, Switzerland) · 2023Review
- Club Cell Secretory Protein in Lung Disease: Emerging Concepts and Potential Therapeutics.Annual review of medicine · 2023Review
- Raised Serum Markers of T Cell Activation and Exhaustion in Granulomatous-Lymphocytic Interstitial Lung Disease in Common Variable Immunodeficiency.Journal of clinical immunology · 2022Article
- Allergic airway recall responses require IL-9 from resident memory CD4Science immunology · 2022Article
- Brief Research Report: Serum clara cell 16 kDa protein levels are increased in patients hospitalized for severe SARS-CoV-2 or sepsis infection.Frontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a devastating disease of unknown etiology. The pathogenic mechanisms are unclear, but evidence indicates that aberrantly activated alveolar epithelial cells secrete a variety of mediators which induce the migration, proliferation and activation of fibroblasts and finally the excessive accumulation of extracellular matrix with the consequent destruction of the lung parenchyma. CC16 (approved symbol SCGB1A1), a putative anti-inflammatory protein produced by "club" cells in the distal airways, has not been evaluated in IPF lungs. In this study, we determined the serum and bronchoalveolar lavage (BAL) levels as well as the lung cell localization of this protein. Also, we explored the usefulness of serum levels of CC16 for the differential diagnosis of IPF (n = 85), compared with non-IPF interstitial lung diseases [chronic hypersensitivity pneumonitis (cHP; n = 85) and connective tissue diseases (CTD-ILD; n = 85)]. CC16 was significantly increased in serum and BAL fluids of IPF patients and was found not only in club cells but also in alveolar epithelial cells. When compared with non-IPF patients and controls, serum levels were significantly increased (p<0.0001). Sensitivity and specificity for CC16 (cut-off 41ng/mL) were 24% and 90%, positive predictive value 56% and negative predictive value 69%. These findings demonstrate that CC16 is upregulated in IPF patients suggesting that may participate in its pathogenesis. Although higher than the serum levels of non-IPF patients it shows modest sensitivity to be useful as a potential biomarker for the differential diagnosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.