Epigenetic Modifications in Asthma Management and Diagnostics: the Current Status and the Progress

Asthma is a complex disorder involving a combination of chronic airway inflammation, intermittent airflow obstruction, and bronchial hyperresponsiveness. This disease, often severe and even life-threatening, places a very serious burden on the patient, and even in milder cases can significantly reduce quality of life. Substantial socioeconomic burden of asthma includes significant direct healthcare costs and even larger indirect costs like lost income and lower productivity, disproportionately affecting low-income and minority groups. Asthma has many faces, differing in terms of clinical symptoms (phenotypes) and underlying mechanisms (endotypes). They can be roughly divided into type 2 (allergic) asthma and non-/low-type 2 (less allergic or non-allergic) asthma. Optimal treatment of diseases, including asthma, requires an individualized approach involving the use of drugs that specifically interfere with underlying mechanisms, as well as the use of biomarkers to identify patients who will respond to such treatment. Therefore, ongoing research aims to identify the precise mechanisms in individual types of asthma in order to establish better biomarkers and detect targets for new drugs. There are particular gaps and therefore considerable scope for improvement in the case of non-/low-type 2 asthma types. In addition, it is necessary to define which epigenetic modifications can be detected after treatment, and when disease modification can be achieved, those related with clinical remission and after allergen hyposensitization. Lifestyle and nutrition can also largely impact epigenetic landscapes in immune and lung cells and key modifications associated with or induced by certain exposures need to be analyzed.

Asthma develops as a result of complex interactions between genetic and environmental factors, with the latter including both risk factors (e.g., environmental pollution) and protective factors (e.g., early exposure to certain microorganisms). The influence of environmental factors is regulated at the molecular level, at least in part, by epigenetic mechanisms. Epigenetic mechanisms are processes that alter gene expression without changing the underlying DNA sequence. Key epigenetic modifications include DNA methylation, in which a methyl group is added to DNA, and histone modifications, which involves chemical changes (e.g. acetylation, methylation, phosphorylation) to the proteins around which DNA is wrapped. Another mechanism is non-coding RNA (e.g. microRNA [miRNA]) or direct mRNA modifications, which control gene expression at the mRNA level. Although these effects play the most significant role in the perinatal period, epigenetic modifications contribute to the pathophysiology of asthma at every stage of the disease.

Integration of genetic and epigenetic investigations with proteomic and metabolomic analyses can provide insights not only in altered pathways but also in potential biomarkers or targets for new mechanism-specific drugs. Indeed, studies conducted on humans and animal models suggest significant potential for epigenetic changes, e.g., DNA methylation or miRNAs, as potential biomarkers of various forms of asthma or related traits. On the other hand, the possibilities of therapeutically influencing epigenetic marks in asthma, e.g., on enzymes controlling histone modification, are becoming apparent.

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Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Clinical Trial
• Community Case Study
• Editorial
• FAIR² Data
• FAIR² DATA Direct Submission
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Review
• Study Protocol
• Systematic Review

Keywords: Epigenetics; Epigenetic modification; DNA methylation; Histone modification; Histone acetylation; Histone methylation; Non-coding RNAs (ncRNAs); MicroRNAs (miRNAs); mRNA modifications; Asthma; Allergy; Atopy; Atopic sensitisation; Phenotype; Endotype; Air

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