Recently, a study published in the international journal Nature Communications reported that scientists from the National Jewish Medical Center and other institutions have found through research that a large number of genetic risks that trigger asthma may be mediated by changes in gene expression in airway epithelial cells. The researchers aimed to identify genetic mutations that trigger asthma by altering the function of airway cells.
Researcher Max A. Seibold, Ph.D., said the study may help identify targeted pathways that can be used to intervene in the development of asthma, thereby blocking the excess secretion of mucus and the development of type 2 airway inflammation, which may exacerbate the development of airway inflammation. Allergic reactions in asthma. Mucus is a hazard that affects human survival and plays an important role in a variety of health conditions, from the common cold and COVID-19 to chronic lung diseases such as asthma and COPD, the more we know about the causes of these diseases, the better researchers will be able to develop new and effective treatments.
In this study, the researchers conducted the first airway transcriptome association study (TWAS) in children and adults with asthma. The first step in conducting this research is to build special models to help predict how an individual organism’s genes function in specific tissues, based solely on their genetic characteristics. Using nasal airway samples and genetic data from a cohort of 700 children in Puerto Rico, either otherwise healthy or with asthma, investigator Seibold and colleagues created these study models for airway tissue.
The researchers then applied these models to genetic data from more than 300,000 participants in the UK Biobank study, a large-scale biomedical database and research repository, which may help them shed light on whether airway genes Genetic alterations in function are associated with the body’s risk of developing asthma. The researchers found that more than one-third of the identified genetic risk factors for asthma may mediate the risk of developing asthma by altering the function of cells lining the airways.
In particular, the researchers identified genetic alterations in a gene that forms mucus structures (MUC5AC) and another gene known to be produced by mucus-secreting cells (FOXA3). The study is the first time researchers have identified a genetic mutation that affects asthma risk by altering mucosal secretory function. In addition, the researchers found that genetic alterations in some key genes in type 2 inflammatory pathway may increase gene expression in the airways, thereby increasing the risk of asthma.
These findings suggest that data on gene expression in individual organisms from genome-wide association studies may shed light on their biological functions and explain that certain genes may be expressed at different levels in different tissues. Studies such as these may help researchers further their research to develop new personalized drug therapies for asthma and other common diseases.
Asthma is a major health threat to the health of the American population. The CDC estimates that about 26.5 million people in the United States suffer from this disease, and 1 in 13 people suffer from this disease. In a short, the results of this study reveal novel genetic and molecular mechanisms of airway mucosal pathology in the body.