Here, we assessed whether TGF-β1 affects the ability of HASM cells to relax in response to β<sub>2</sub>-agonists, a mainstay treatment for airway hyperresponsiveness in asthma.
Immunohistochemistry was used to measure collagen III deposition and TGF-beta(1) expression in biopsies from patients with long-standing asthma treated with inhaled corticosteroids, patients with recently diagnosed asthma, and control subjects.
In conclusion, the results suggested that TGF-β1 enhances ADAM33 expression in airway epithelial cells, and that ADAM33 induces the EMT of airway epithelial cells, thus participating in airway remodeling in asthma.
In conclusion, these results suggest a role of TGF-β1 in olive-pollen sensitization and TNF-α and IL-10 genotypes in the asthma induced by specific olive-pollen allergens.
In T cells only patients with moderate asthma showed increased activin A mRNA expression, whereas TGF-beta(1) expression was equal to that seen in healthy subjects.
In the current study, we found that miR-448-5p was dramatically decreased in lung tissues of asthmatic mice and TGF-β1-stimulated bronchial epithelial cells.
In the present study, we confirmed the association of rs1800469 in TGF-beta1 and rs20541 in IL-13 with asthma and found a trend toward association between rs2241712 in TGF-beta1 and rs2070874 in IL-4 with asthma among atopic subjects, suggesting TGF-beta1, IL-4 and IL-13 may be associated with the susceptibility and development of asthma in this Chinese population.
Interestingly, a novel 3-locus haplotype, 23_G_T, was found to be significantly associated with asthma (P = .00001 in cohorts A and B) as well as with higher serum TGF-beta1 level (P = .01).
It will further review the evidence demonstrating the extent to which IL-17A interacts with various immune factors, specifically TGF-β1, to contribute to ASM remodeling and altered function in T<sub>H</sub>17-driven endotypes of severe asthma.
MicroRNA-744 Inhibits Proliferation of Bronchial Epithelial Cells by Regulating Smad3 Pathway via Targeting Transforming Growth Factor-β1 (TGF-β1) in Severe Asthma.
Multimarker analysis identified TGFB1, IL1RL1, the gene encoding IL-18 receptor 1 (IL18R1), and DPP10 as the genes most significantly associated with asthma.
Our results associating TGFB1 and TLE4 with clinical features of asthma suggest potential application of these parameters in the management of asthma children.
Our results indicate that the polymorphisms at C-509T and T869C of the TGF-beta(1) gene are associated with asthma susceptibility in atopic subjects of the Hong Kong Chinese population, and the C-509T polymorphism may play a role in the pathogenesis of airflow obstruction.
Primary human bronchial fibroblasts (HBFs) propagated from ex vivo bronchial biopsies derived from patients with diagnosed asthma and human embryonic lung IMR-90 fibroblasts were cultured in vitro and treated with TGF-β1 and apigenin.