IL-17A-neutralizing antibody ameliorates inflammation and fibrosis in rosacea by antagonizing the CXCL5/CXCR2 axis.
Zhang. Chuanxi C; Jin. Hui H; Kang. Yumeng Y; Wu. Yiling Y; Zheng. Ruiping R; Zhang. Ziyan Z; Xu. Hong H; Cai. Wenchen W; Gao. Xuemin X; Liu. Heliang H; Mao. Na N; Yang. Jie J
Key Findings
- IL‑17A‑neutralizing antibodies lowered skin thickness and inflammation in LL‑37‑induced rosacea mice
- Treatment decreased inflammatory markers (TNF‑α, CAMP, TLR4, NF‑κB) and angiogenesis factors (CD31, VEGF)
- Blocking IL‑17A suppressed the CXCL5/CXCR2 signaling axis and reduced fibrosis markers like COL1 and TGF‑β1
Practical Outcomes
- For self‑experimenters, the work hints that IL‑17A is a key driver of rosacea inflammation and scarring, but the effective agents are clinical antibodies, not something you can safely use at home. No actionable dosing or over‑the‑counter protocol emerges from this mouse study.
Summary
In mice, blocking the immune protein IL‑17A with special antibodies reduced skin inflammation and scarring caused by the peptide LL‑37, which is used to mimic rosacea. The study shows a possible way to calm rosacea‑related damage, but it involves prescription‑only antibodies and isn’t a DIY approach.
Abstract
Rosacea is a chronic inflammatory skin disorder that can lead to fibrosis. However, the mechanisms underlying fibrosis in the later stages of rosacea have been less thoroughly investigated. Interleukin-17A (IL-17A) has been implicated in both inflammation and organ fibrosis; however, the effectiveness and mechanism of IL-17A-neutralizing antibodies in the later stages of rosacea-related fibrosis remain unclear. In this study, we induced rosacea-like lesions in mice using LL-37 and administered IL-17A-neutralizing antibodies. The results indicated that the IL-17A-neutralizing antibodies alleviated skin damage, reduced skin thickness, and decreased the secretion of inflammatory factors (TNF-α, CAMP, TLR4, P-NF-kB), angiogenesis-related factors (CD31, VEGF), and the TGF-β1 signaling pathway, along with factors associated with epithelial-mesenchymal transition and the deposition of fibrosis-related proteins (COL1) in the rosacea-like mouse models. Furthermore, the IL-17A-neutralizing antibodies effectively diminished the expression of IL-17, IL-17R, CXCL5, and CXCR2 in the skin. Our findings demonstrate that IL-17A-neutralizing antibodies inhibit the activation of the CXCL5/CXCR2 axis in rosacea-like skin tissue, thereby ameliorating inflammation and fibrosis associated with the condition.
Study Information
pubmed
2024
2024-10-15T00:00:00.000Z
10.1096/fj.202400006r