MicroRNA and heme oxygenase-1 in allergic disease

Int Immunopharmacol. 2020 Mar:80:106132. doi: 10.1016/j.intimp.2019.106132. Epub 2020 Jan 22.

Abstract

Background: Cumulative evidence suggests that in allergic diseases, oxidative stress and inflammation could often be detected. Therefore, the antioxidant/anti-inflammatory heme oxygenase (HO)-1 was recognized as a protective factor in allergic disorders. However, the precise underlying mechanisms of HO-1-based protection are not yet completely understood. In addition, miRNAs, a class of non-coding RNA, have been confirmed to associate with immunologic and inflammatory disorders in allergy recently. In addition, abundant studies have verified there is a complex connection between HO-1 and miRNAs. Thus, in this review, the combination of HO-1 and miRNAs (e.g. miR-155) in anti-allergy would be introduced.

Methods: To further confirm our hypothesis, GEO sequencing datasets of atopic dermatitis children were analyzed. The miR-548a-3p might regulate the cellular response to hydrogen peroxide through HO-1 and HIF-1pathway. Meanwhile, this article reviews the latest knowledge and studies on the protective mechanisms of miRNA-HO-1 in allergy.

Results: In brief, we supposed that miRNAs/HO-1 could mediate allergy through oxidative stress pathways, transcription factors and immune cell functions such as mast cell maturation, chemokine expression in T cell and dendritic cell degranulation. Although the detailed mechanism needs further research, this review may reveal the potential application of miRNAs and HO-1 in genetic therapies of allergic disease and provide new biomarkers.

Conclusion: This article examines the latest knowledge and studies on the protective roles and mechanisms of miRNA-HO-1 in allergy. Moreover, via bioinformatics analysis of GEO dataset, it was demonstrated that miRNAs (e.g. miR-205, miR-203, and miR-483-5p) could regulate allergy process through HO-1.

Keywords: Allergic disease; Atopic dermatitis; HO-1; Immunoreaction; Oxidative stress; miRNA.

Publication types

  • Review

MeSH terms

  • Animals
  • Computational Biology
  • Datasets as Topic
  • Disease Models, Animal
  • Genetic Therapy / methods
  • Heme Oxygenase-1 / genetics*
  • Heme Oxygenase-1 / metabolism
  • Humans
  • Hypersensitivity / genetics*
  • Hypersensitivity / immunology
  • Hypersensitivity / therapy
  • Hypoxia-Inducible Factor 1 / genetics
  • Hypoxia-Inducible Factor 1 / metabolism
  • MicroRNAs / metabolism*
  • Oxidative Stress / genetics
  • Oxidative Stress / immunology
  • Protective Factors
  • Signal Transduction / genetics*
  • Signal Transduction / immunology

Substances

  • Hypoxia-Inducible Factor 1
  • MicroRNAs
  • Heme Oxygenase-1