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Lysozyme modulates inflammatory responses to exacerbate the severity of rheumatoid arthritis
Hao Xu1, Luxu Yin2, Liang Zou3
1Biomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Background:
The mechanisms underlying Rheumatoid Arthritis (RA) remain unclear. Despite having relatively well-defined treatment strategies, current therapeutic approaches only achieve a remission rate of 70 %-80 %, with poor prognosis and no clear diagnostic criteria for early RA. Therefore, there is a need for new therapeutic targets or biomarkers to improve the treatment of RA.
Methods:
Firstly, we identified the expression characteristics of lysozyme (LYZ) in early RA patients through plasma proteomics and synovial fluid single-cell sequencing analysis. Secondly, we constructed Lyz1 cKO mice to investigate the role of Lyz1 in RA pathogenesis using the Collagen Antibody-Induced Arthritis (CAIA) mouse model. Thirdly, we silenced LYZ to clarify its impact on TNF-α-induced inflammatory cytokine release and other inflammatory phenotypes in MH7A cells. Finally, we explored the cellular pathways involving LYZ in fibroblast-like synoviocytes (FLSs) and changes in RA-related genes through RNA sequencing (RNA-Seq).
Results:
LYZ was highly expressed in the plasma and synovial macrophages of early RA patients. The absence of Lyz1 reduced the arthritis course and joint damage in CAIA mice. Silencing LYZ promoted the proliferation and apoptosis of MH7A cells and improved their inflammatory phenotypes, possibly through the regulation of the TNF signaling pathway.
Conclusion:
LYZ is highly expressed in the plasma and synovial fluid macrophages of early RA patients and exacerbates RA progression by modulating inflammation-related pathways, demonstrating potential as a biomarker for early RA diagnosis or a therapeutic target.
Insights
Lysozyme (LYZ) is elevated in early Rheumatoid Arthritis (RA) patients, worsening joint damage and inflammation. Targeting LYZ may offer new diagnostic and therapeutic strategies for RA.
Area of Science:
- Immunology
- Molecular Biology
- Rheumatology
Background:
- Rheumatoid Arthritis (RA) pathogenesis remains incompletely understood, with current treatments achieving suboptimal remission rates.
- Existing RA therapies have limitations, including a lack of clear early diagnostic criteria and a significant portion of patients not achieving remission.
- There is a critical need for novel therapeutic targets and biomarkers to enhance early RA diagnosis and treatment efficacy.
Purpose of the Study:
- To investigate the role of lysozyme (LYZ) in Rheumatoid Arthritis (RA) pathogenesis.
- To determine if LYZ can serve as a diagnostic biomarker or therapeutic target for early RA.
- To elucidate the molecular mechanisms by which LYZ influences RA progression.
Main Methods:
- Plasma proteomics and synovial fluid single-cell sequencing identified LYZ expression in early RA patients.
- Lyz1 conditional knockout (cKO) mice were used to assess LYZ's role in a Collagen Antibody-Induced Arthritis (CAIA) model.
- In vitro studies silenced LYZ in MH7A cells to evaluate its effect on TNF-α-induced inflammatory responses.
- RNA sequencing (RNA-Seq) explored LYZ-associated cellular pathways in fibroblast-like synoviocytes (FLSs).
Main Results:
- Lysozyme (LYZ) exhibited high expression in the plasma and synovial macrophages of early RA patients.
- Mice lacking Lyz1 showed a reduced course of arthritis and diminished joint damage in the CAIA model.
- Silencing LYZ in MH7A cells modulated TNF signaling, affecting inflammatory cytokine release, cell proliferation, and apoptosis.
Conclusions:
- Lysozyme (LYZ) is significantly upregulated in early RA patients, correlating with disease progression.
- LYZ exacerbates RA pathogenesis by modulating inflammation-related pathways, particularly TNF signaling.
- LYZ presents potential as a valuable biomarker for early RA diagnosis and a promising therapeutic target for RA intervention.
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