Bioinformatics Analysis and Animal Experiments Revealed the Potential Role of IGFBP3 in Allergic Rhinitis.

Area of Science:

• Immunology
• Molecular Biology
• Bioinformatics

Background:

• Allergic rhinitis (AR) is a common chronic inflammatory condition significantly impacting quality of life.
• The molecular mechanisms of AR, particularly the role of hypoxia-associated genes, are not fully understood.
• Investigating novel therapeutic targets for AR is crucial due to the limitations of current treatments.

Purpose of the Study:

• To identify hypoxia-related genes differentially expressed in allergic rhinitis (AR) using bioinformatics.
• To investigate the role of insulin-like growth factor-binding protein 3 (IGFBP3) in AR pathogenesis.
• To evaluate the therapeutic potential of IGFBP3 in an AR mouse model.

Main Methods:

• Comprehensive bioinformatics analysis of human and mouse gene expression datasets (GSE261239, GSE171005).
• Identification of hypoxia-related genes using curated databases and construction of protein-protein interaction networks.
• Validation in an ovalbumin-induced mouse model of AR, including assessment of IGFBP3 treatment.

Main Results:

• Eleven hypoxia-related genes were differentially expressed in AR, with IGFBP3 identified as a downregulated hub gene.
• Reduced IGFBP3 expression correlated with decreased mast cell and Th1 cell infiltration.
• Recombinant IGFBP3 treatment significantly reduced AR symptoms, serum IgE levels, and nasal inflammation in mice.

Conclusions:

• IGFBP3 plays a critical regulatory role in AR pathogenesis, potentially by influencing the hypoxic microenvironment and immune cell activity.
• IGFBP3 treatment effectively mitigated allergic symptoms and restored nasal tissue integrity in a mouse model.
• IGFBP3 represents a promising novel therapeutic target for allergic rhinitis.