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S100A9 Exacerbates the Inflammation in Rosacea through Toll-Like Receptor 4/MyD88/NF-κB Signaling Pathway
Yan Le1, Jiawen Zhang1, Yi Lin1
1Department of Dermatology, Huashan Hospital of Fudan University, Shanghai, China.
The Journal of Investigative Dermatology
|March 6, 2024
Summary
S100A9, a key inflammatory protein, is elevated in rosacea patients and promotes skin inflammation by activating specific signaling pathways. Inhibiting S100A9 reduces rosacea symptoms, offering new therapeutic targets.
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Rosacea is a chronic inflammatory skin condition.
- S100A9 is a known proinflammatory alarmin implicated in other inflammatory diseases.
- The role of S100A9 in rosacea pathogenesis is currently unknown.
Purpose of the Study:
- To investigate the role of S100A9 in rosacea.
- To elucidate the molecular mechanisms underlying S100A9's involvement in rosacea.
Main Methods:
- Measured S100A9 expression in rosacea patients and a mouse model.
- Correlated S100A9 levels with disease severity and inflammatory markers.
- Investigated S100A9's effect on inflammatory factor production in vitro.
- Examined the impact of S100A9 inhibition on rosacea-like dermatitis in vivo.
Main Results:
- S100A9 expression was significantly upregulated in rosacea lesions and serum.
- Elevated S100A9 correlated with increased disease severity and inflammatory cytokines.
- S100A9 activation of TLR4/MyD88/NF-κB pathways promoted inflammation.
- S100A9 inhibition ameliorated rosacea-like dermatitis and inflammation.
Conclusions:
- S100A9 plays a crucial role in rosacea pathogenesis.
- S100A9 promotes skin inflammation via the TLR4/MyD88/NF-κB pathway.
- Targeting S100A9 presents a potential therapeutic strategy for rosacea.
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