ArticleImmunity, inflammation and disease2024
The functional role of CST1 and CCL26 in asthma development.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 6 citations in OpenAlex.
- Unique nasal cell states induced by common pediatric respiratory viruses.bioRxiv : the preprint server for biology · 2026Article
- Helper T cells and chemokines in elderly asthma - Mechanisms of airway inflammation and remodeling: A review.Biomolecules & biomedicine · 2026Review
- Association Between Serum MPO-DNA and CCL26 Levels and Poor Prognosis in Children with Multidrug-Resistant Organism-Associated Pneumonia.International journal of general medicine · 2026Article
- Predictive value of CCL26 and CCR3 levels for prognosis assessment in children withTranslational pediatrics · 2025Article
- Proteomic Profiling of Inflammatory Protein Dysregulation in HLA-B27-Positive Ankylosing Spondylitis: Molecular Signatures and Potential Biomarkers.Biomolecules · 2025Article
- Transcriptomic Analysis ofPlants (Basel, Switzerland) · 2025Article
- T2 cytokine-driven alarmin and antiviral responses in asthma: insights into immune modulation and the role of IL-4Rα targeting.Frontiers in allergy · 2025Article
- The functional role of CST1 and CCL26 in asthma development.Immunity, inflammation and disease · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundAsthma is the most common chronic disease in children with an increasing prevalence. Its development is caused by genetic and environmental factors and allergic sensitization is a known trigger. Dog allergens affect up to 30% of all children and dog dander-sensitized children show increased expression of cystatin-1 (CST1) and eotaxin-3 (CCL26) in nasal epithelium. The aim of our study was to investigate the functional mechanism of CST1 and CCL26 in the alveolar basal epithelial cell line A549.
methodsA549 cells were transfected with individual overexpression vectors for CST1 and CCL26 and RNA sequencing was performed to examine the transcriptomics. edgeR was used to identify differentially expressed genes (= DEG, |log
resultsThe overexpression of CST1 resulted in a total of 27 DEG (1 upregulated and 26 downregulated) and the overexpression of CCL26 in a total of 137 DEG (0 upregulated and 137 downregulated). The gene ontology enrichment analysis showed a significant downregulation of type I and III interferon signaling pathway genes as well as interferon-stimulated genes. At the protein level, overexpression of CST1 induced a significantly increased expression of CCL3, whereas CCL26 overexpression led to increased expression of HGF, and a decrease of CXCL11, CCL20, CCL3 and CXCL10.
conclusionOur results indicate that an overexpression of CST1 and CCL26 cause a downregulation of interferon related genes and inflammatory proteins. It might cause a higher disease susceptibility, mainly for allergic asthma, as CCL26 is an agonist for CCR-3-carrying cells, such as eosinophils and Th2 lymphocytes, mostly active in allergic asthma.
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.