To determine the contribution of polymorphisms and haplotypes of beta 2-adrenergic receptor with serum IgE levels in children from Argentina with mild, moderate, and severe asthma.
To determine if these polymorphisms contribute to the development of asthma by investigating the associations between the polymorphisms at amino acid positions 16 and 27 of the B2AR gene and asthma-related parameters in a large, phenotypically well-characterized population which was unselected for asthma.
To date, clinical studies suggest that these beta(2)AR polymorphisms may alter asthmatic phenotype and the response to beta-agonist therapy, making these variants the first of undoubtedly several genetic loci that will ultimately be found that will provide for individualized therapy in asthma.
To compare the effectiveness and safety of tiotropium vs LABAs, when used with inhaled corticosteroids (ICS) in black adults with asthma and to determine whether allelic variation at the Arg16Gly locus of the β2-adrenergic receptor (ADRB2) geneis associated with treatment response.
Thus beta2AR polymorphisms act as disease modifiers in asthma and represent one of probably many genetic variables involved in the pathophysiology of asthma.
This study evaluates the utility of autopsy lung for studies of gene expression and examines the hypothesis that increased expression of beta 2 AR mRNA in peripheral lung underlies the increased receptor number reported in central airways in fatal asthma. beta 2AR mRNA levels have been quantitated using the ribonuclease protection assay on RNA from peripheral lung obtained both at autopsy and thoracotomy from subjects with normal lungs as well as subjects with asthma or chronic obstructive pulmonary disease (COPD).
This study evaluated the effect of the beta2-adrenergic receptor (ADRB2) polymorphism on lung function and asthma control with regular use of combination treatment of an inhaled ICS plus LABA.
This single-nucleotide polymorphism is associated with reduced expression of the gene for the β2-adrenergic receptor (ADRB2) in CD4(+) lymphocytes of subjects with asthma, and it affects brain connectivity of the amygdala and the insula (a biomarker of anxiety).
This observation suggests therefore that ADRB2 gene can confer genetic susceptibility to BHR, rather than having only a disease-modifying effect in asthma.
This notion is supported by several reports that have implicated the chromosomal region 5q31-q33 harboring the gene for the beta(2)-adrenoreceptor in the genetics of asthma and related phenotypes.
These results suggest that beta2AR polymorphisms play an important role in the airway responsiveness to inhaled beta2-agonist and the initial asthma onset.
These results indicate that asthma, allergy, and methacholine airway hyperresponsiveness are not linked to a dominant beta(2)-adrenoceptor gene with strong effect in these eight families with an inherited pattern of asthma.
These findings support the potential use of ADRB2 5'-UTR methylation as a biomarker of both asthma severity and risk for NO (2) -associated asthma exacerbations in children, and present the first evidence of an epigenetic link between an important environmental exposure and childhood asthma severity.
Therefore, ADRB2 polymorphisms are an important consideration in assessing individual patients with difficult asthma that may be drug-induced for reasons of ADRB2 genotype.
The results demonstrate that GL and SA have synergistic anti-asthmatic effects and offer the possibility of a therapeutic application of GL in combination with beta(2)-AR agonists in the treatment of asthma.
The related papers on ADRB2 polymorphisms and asthma were systematically reviewed in databases of PubMed, EMBASE, Cochrane Library, and WanFang, Odds ratios (ORs) and corresponding 95% confidence intervals (95% CIs) were measured.
The primary hypothesis was that severe asthma exacerbations requiring hospital admission were associated with rare ADRB2 variants in patients receiving LABA therapy.