LINC00998 Modulating M2 Macrophage Activation in Allergic Rhinitis by Stabilizing BOB.1 mRNA

Area of Science:

• Immunology
• Molecular Biology
• Genetics

Background:

• Allergic rhinitis (AR) presents a growing global health challenge with significant socioeconomic impact.
• Long noncoding RNAs (lncRNAs) are increasingly recognized for their role in allergic responses.
• This study investigates the specific involvement of lncRNA LINC00998 in the mechanisms underlying AR.

Purpose of the Study:

• To explore the role of lncRNA LINC00998 in the pathogenesis of allergic rhinitis (AR).
• To investigate the relationship between LINC00998 expression and macrophage polarization in AR.
• To elucidate the molecular mechanism by which LINC00998 influences macrophage polarization.

Main Methods:

• Assessed LINC00998 expression in peripheral blood mononuclear cells from AR patients using qRT-PCR.
• Utilized in vitro models (THP-1 cells, primary human macrophages) and an AR mouse model to study macrophage polarization.
• Employed gain- and loss-of-function experiments, qRT-PCR, flow cytometry, and Western blot to analyze LINC00998's mechanism.

Main Results:

• LINC00998 expression was significantly decreased in AR patients and M2 macrophages.
• Suppression of LINC00998 enhanced M2 polarization, while overexpression attenuated it.
• LINC00998 regulated BOB.1 expression, which in turn modulated macrophage polarization via the PU.1/IL-1β axis.

Conclusions:

• The lncRNA LINC00998 plays a crucial role in modulating M2 macrophage polarization in allergic rhinitis.
• LINC00998 exerts its effects by regulating the BOB.1/PU.1/IL-1β signaling pathway.
• These findings provide novel insights into AR pathogenesis and potential therapeutic targets.