Non‐coding RNA LINC01010 regulates macrophage polarization and innate immune functions by modulating NFκB signaling pathway

Innate immune response is regulated by tissue resident or infiltrating immune cells such as macrophages (Mφ) that play critical role in tissue development, homeostasis, and repair of damaged tissue. However, the epigenetic mechanisms that regulate Mφ plasticity and innate immune functions are not we...

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Bibliographic Details
Published in:Journal of cellular physiology 2024-05, Vol.239 (5), p.e31225-n/a
Main Authors: Valverde, Araceli, Naqvi, Raza Ali, Naqvi, Afsar R.
Format: Article
Language:English
Subjects:
Animals
Antigen processing
Bacteria
Biofilms
Biomarkers
Cell Differentiation - genetics
Cell Line, Tumor
Differentiation
E coli
Epigenetics
Gene Expression Regulation
Homeostasis
Humans
Immune response
Immune system
Immunity, Innate - genetics
Immunological diseases
innate immune response
Innate immunity
Lipopolysaccharides
Lipopolysaccharides - pharmacology
lncRNAs
Lymphocytes
Lymphocytes B
Lymphocytes T
Macrophage Activation - genetics
Macrophages
Macrophages - immunology
Macrophages - metabolism
Mice
Microorganisms
migration
NF-kappa B - metabolism
NF-κB protein
Non-coding RNA
Periodontal disease
Periodontal diseases
Phagocytosis
Polarization
Ribonucleic acid
RNA
RNA, Long Noncoding - genetics
RNA, Long Noncoding - metabolism
RNA-mediated interference
Signal Transduction
Transcriptomes
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Summary:Innate immune response is regulated by tissue resident or infiltrating immune cells such as macrophages (Mφ) that play critical role in tissue development, homeostasis, and repair of damaged tissue. However, the epigenetic mechanisms that regulate Mφ plasticity and innate immune functions are not well understood. Long non‐coding RNA (lncRNA) are among the most abundant class of transcriptome but their function in myeloid cell biology is less explored. In this study, we deciphered the regulatory role of previously uncharacterized lncRNAs in Mφ polarization and innate immune responses. Two lncRNAs showed notable changes in their levels during M1 and M2 Mφ differentiation. Our findings indicate that LINC01010 expression increased and AC007032 expression decreased significantly. LINC01010 exhibit myeloid cell‐specificity, while AC007032.1 is ubiquitous and expressed in both myeloid and lymphoid (T cells, B cells and NK cells) cells. Expression of these lncRNAs is dysregulated in periodontal disease (PD), a microbial biofilm‐induced immune disease, and responsive to lipopolysaccharide (LPS) from different oral and non‐oral bacteria. Knockdown of LINC01010 but not AC007032.1 reduced the surface expression of Mφ differentiation markers CD206 and CD68, and M1Mφ polarization markers MHCII and CD32. Furthermore, LINC01010 RNAi attenuated bacterial phagocytosis, antigen processing and cytokine secretion suggesting its key function in innate immunity. Mechanistically, LINC01010 knockdown Mφ treated with Escherichia coli LPS exhibit significantly reduced expression of multiple nuclear factor kappa B pathway genes. Together, our data highlight functional role of a PD‐associated lncRNA LINC01010 in shaping macrophage differentiation, polarization, and innate immune activation. Long non‐coding RNA LINC01010 expression is increased during M1 and M2 polarized monocyte‐derived macrophage differentiation and exhibits impaired expression in inflamed gingiva. Knockdown of LINC01010 downregulated M1Mφ phenotype markers and attenuated bacterial phagocytosis, antigen processing and cytokine secretion. LINC01010 RNAi impaired NFκB signaling in Mφ treated with E. coli LPS suggesting its key function in innate immunity.
ISSN:0021-9541
1097-4652
1097-4652
DOI:10.1002/jcp.31225