ArticleMediators of inflammation2013
Transforming growth factor β1 genotypes in relation to TGFβ1, interleukin-8, and tumor necrosis factor alpha in induced sputum and blood in cystic fibrosis.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04242420 (Impact of Connexin 37, Connexin 43 on Clinical Disease Phenotype in Delta F508 Homozygous Patients With Cystic Fibrosis), which is not on this map. Cited by 8 papers.
What it found
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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.
Impact of Connexin 37, Connexin 43 on Clinical Disease Phenotype in Delta F508 Homozygous Patients With Cystic Fibrosis (CF) (CF-Modifier)
Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Epithelial-Mesenchymal Transition Mechanisms in Chronic Airway Diseases: A Common Process to Target?International journal of molecular sciences · 2023Review
- Recruited monocytes/macrophages drive pulmonary neutrophilic inflammation and irreversible lung tissue remodeling in cystic fibrosis.Cell reports · 2022Article
- The effect of TGF-βBMC pulmonary medicine · 2022Article
- Article
- Impact of aFrontiers in genetics · 2020Article
- Transforming Growth Factor-β1 Selectively Recruits microRNAs to the RNA-Induced Silencing Complex and Degrades CFTR mRNA under Permissive Conditions in Human Bronchial Epithelial Cells.International journal of molecular sciences · 2019Article
- Pro-resolving lipid mediator Resolvin D1 serves as a marker of lung disease in cystic fibrosis.PloS one · 2017Article
- Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHigh-producer TGFβ1 genotypes are associated with severe lung disease in cystic fibrosis (CF), but studies combining IL-8, TNFα-, and TGFβ1(+genotype) levels and their impact on CF lung disease are scarce.
aimAssessing the relationship between TGF β 1, IL-8, and TNF- α and lung disease in CF in an exacerbation-free interval.
methodsTwenty four patients delta F508 homozygous (median age 20.5 y, Shwachman score 75, FEV1(%) 83) and 8 controls (median age 27.5 y) were examined. TGF β 1 was assessed in serum and induced sputum (IS) by ELISA, for IL-8 and TNF- α by chemiluminescence in IS and whole blood. Genotyping was performed for TGF β 1 C-509T and T+869C utilizing RFLP.
resultsTGF β 1 in IS (CF/controls median 76.5/59.1 pg/mL, P < 0.074) was higher in CF. There was a negative correlation between TGF β 1 in serum and lung function (LF) (FEV1 (r = -0.488, P = 0.025), MEF 25 (r = -0.425, P = 0.055), and VC (r = -0.572, P = 0.007)). Genotypes had no impact on TGF β 1 in IS, serum, and LF. In IS TGF β 1 correlated with IL-8 (r = 0.593, P < 0.007) and TNF- α (r = 0.536, P < 0.018) in patients colonized by bacteria with flagellin.
conclusionTGF β 1 in serum not in IS correlates with LF. In patients colonized by bacteria with flagellin, TGF β 1 correlates with IL-8 and TNF- α in IS.
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