Expression of vitamin D receptor in bronchial asthma and its bioinformatics prediction

Abstract

Vitamin D receptors (VDRs) are associated with the occurrence and development of asthma. The aim of the present study was to analyze the secondary structure and B-cell and T-cell epitopes of VDR using online prediction software and aid in the future development of a highly efficient epitope-based vaccine against asthma. Blood samples were collected from peripheral blood of asthmatic children. Reverse transcription quantitative-polymerase chain reaction (RT-qPCR) was performed to detect the expression of VDR in the peripheral blood. Mouse models of asthma were established. Hematoxylin and eosin staining was performed to observe the pathological alterations of the lungs of mice. Immunohistochemistry, western blot analysis and RT-qPCR were performed to detect the expression of VDR in the lungs of asthmatic mice. Online prediction software immune epitope database and analysis resource, SYFPEITHI and linear epitope prediction based on propensity scale and support vector machines were used to predict the B-cell and T-cell epitopes and the RasMol and 3DLigandSite were used to analyze the tertiary structure of VDR. RT-qPCR demonstrated that VDR expression in the peripheral blood of asthmatic children was decreased. Immunohistochemistry, western blotting and RT-qPCR demonstrated that VDR expression also decreased in the lungs of mouse models of asthma. VDR B-cell epitopes were identified at 37–45, 88–94, 123–131, 231–239, 286–294 and 342–350 positions of the amino acid sequence and VDR T-cell epitopes were identified at 125–130, 231–239 and 265–272 positions. A total of six B-cell epitopes and three T-cell epitopes for VDR were predicted by bioinformatics, which when validated, may in the future aid in immunological diagnosis and development of a targeted drug therapy for clinical asthma.

Dioscin exhibits protective effects on in vivo and in vitro asthma models via suppressing TGF‐β1/Smad2/3 and AKT pathways

“…[52] Several studies have reported that TGF-β1 exhibits an important role in the remodeling of the airway and is involved in multiple cellular processes, such as smooth muscle remodeling, fibrosis, and microvascular alternations. [53][54][55] Activation of TGF-β leads to phosphorylation of Smads. [56] The elevated TGF-β1 and p-Smad2/3 took part in fibrosis and inflammation in mice with OVA-induced asthma.…”

“…[53] Administration of a TGF-β1 receptor inhibitor significantly elevated IL-6, TNF-α, and IL-17a but decreased IL-10, thus reversing the protective effect of epigallocatechin gallate against airway inflammation in asthmatic mice. [54] In addition to the classical TGF-β1/Smad signaling, PI3K/AKT signaling and its cross-talk with TGF-β also plays a role in inflammation and airway remodeling in asthma. [29,30] In the lung tissues of OVA mice, the PI3K/AKT signaling pathway was activated, and inhibition of PI3K/AKT signaling attenuated allergic airway inflammation in asthmatic mice.…”

Autophagy‐related 5 gene mRNA expression and ATG5 rs510432 polymorphism in children with bronchial asthma

“…Its incidence and mortality have risen in recent years 1 . To improve its burden, studies have been directed to understand its pathogenesis which is complex and depends upon the interaction of genetic, environmental, and hormonal factors 2 . We are in a new era in personalized asthma treatment according to each patient's phenotype and his/her underlying pathophysiology and genetics 3 …”