Eosinophils enhance WNT-5a and TGF-β1 genes expression in airway smooth muscle cells and promote their proliferation by increased extracellular matrix proteins production in asthma.
These studies demonstrate that GSDMB, a gene highly linked to asthma but whose function in asthma is previously unknown, regulates AHR and airway remodeling without airway inflammation through a previously unrecognized pathway in which GSDMB induces 5-LO to induce TGF-β1 in bronchial epithelium.
The aim of this study was to analyze common TGFB1 gene promoter polymorphisms C-509T and G-800A in Serbian asthmatics and to investigate their association with exacerbations.
The aim of the present study was to identify polymorphic forms of the nuclear receptor subfamily 3, group C, member 1 (NR3C1) and transforming growth factor β1 (TGF-β1) genes and evaluate their impact on the expression levels of interleukin (IL)-5 and IL‑15 in asthma.
Therefore, we here developed a mouse model of asthma by microinjecting the pronucleus with a vector spontaneously coding human IL10 and TGFB1 gene to explore the possible interaction between these two potent molecules during asthma progression.
Associations between TGF-β and eosinophils will be addressed and the effects of genetic polymorphisms of the TGF-β1 gene explored in the context of asthma.
To derive a more precise estimation of the relationship between the T869C and C-509T polymorphisms of the TGF-β1 gene and asthma, a meta-analysis of 24 published case-control studies was conducted.
This study evaluated the role and frequency of genetic polymorphisms (C-509T, C+466T and T+869C) of the TGF-β1 gene in the study group (patients with asthma) and the control group (healthy volunteers).
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.
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.
This study compared the expression of PI3K isoforms by ASM cells from donors with asthma (A), chronic obstructive pulmonary disease (COPD), or neither disease (NA), and investigated the role of PI3K isoforms in the production of TGFβ1 induced pro-inflammatory cytokine and contractile proteins in ASM cells.
TGF-β1 activation was also greater in children with severe asthma and was associated with higher airway 8-isoprostane, malondialdehyde, and IL-13 concentrations.
We investigated the interactive effects of 11 innate immunity-related genes (IL10, IL12b, IL8, TLR2, TLR4, CD14, IFNGR, CC16, IFNg, CMA1, and TGFB) and four IgE response genes (IL4, IL13, IL4RA, and STAT6) with 'Western' or 'Eastern' environments/lifestyles on asthma and allergy in Karelian children.
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.
Transforming growth factor beta 1 (TGF-beta1) is a major participant in the airway remodeling of asthma, a component of cellular stress response pathways, and enhanced epithelial immunoreactivity is known to occur in allergic rhinitis.