Two probiotic strains reduced rosacea-like skin inflammation in mice by suppressing the TLR2/MyD88/NF-κB signaling pathway and lowering LL-37 expression.
Combination was most effectiveUsing both probiotic strains together produced better results than either strain alone for reducing rosacea-like inflammation
What the researchers found
Both L. salivarius 23-006 and L. paracasei 23-008 reduced skin lesions, skin inflammatory infiltrates, and inflammatory factor expression in the LL-37 rosacea mouse model. The combination of both strains produced the strongest effects.
The probiotics worked by inhibiting the TLR2/MyD88/NF-kB signaling pathway, which is the same pathway LL-37 uses to trigger rosacea inflammation. They also reduced cathelicidin LL-37 expression itself, breaking the cycle. Gut microbiome analysis showed the probiotics increased Lactobacillus levels while reducing Coprococcus and Oscillospira, and strengthened the intestinal barrier.
Postbiotics (the metabolic byproducts of the bacteria, used without live bacteria) also helped but were less effective than live probiotic treatment.
Why it matters
Rosacea affects roughly 5% of the global population and is difficult to treat. LL-37 (cathelicidin) is overexpressed in rosacea skin and drives inflammation. The gut-skin axis is an emerging concept suggesting that gut bacteria influence skin conditions. This study provides a mechanistic link between probiotic gut treatment and skin improvement in a rosacea model.
The numbers in context
- Two strains tested: L. salivarius 23-006 and L. paracasei 23-008
- Combination treatment was most effective
- TLR2/MyD88/NF-kB pathway was inhibited
- LL-37 expression reduced in treated mice
- Lactobacillus abundance increased; Coprococcus and Oscillospira decreased
- Postbiotics were less effective than live probiotics
How the study worked
Researchers isolated L. salivarius 23-006 and L. paracasei 23-008 from healthy human volunteer feces. They created rosacea-like skin inflammation in mice by injecting LL-37 peptide. Mice were treated with individual probiotics, the combination, or postbiotics. They measured skin inflammation, inflammatory markers, LL-37 expression, TLR2/MyD88/NF-kB pathway activity, and gut microbiome composition via 16S rRNA sequencing.
Who was studied
Mice with LL-37-induced rosacea-like skin inflammation
What this study cannot tell us
This was tested in mice, not people. The LL-37 injection model creates rosacea-like symptoms but is not the same as human rosacea, which develops over years. The probiotic strains were from healthy volunteers and may not work the same in rosacea patients. The gut-to-skin mechanism is demonstrated in mice but not confirmed in humans. Postbiotics were less effective, which limits the shelf-stable product potential.
How to read the evidence
Rated preliminary: animal study using a rosacea model that mimics but does not replicate human disease. No human data yet.
When this study was published
Published in 2024. The gut-skin axis is an active research area with growing interest in probiotic interventions for skin conditions.
The bigger picture
LL-37 is overexpressed in rosacea skin and drives the inflammatory cascade. The gut-skin axis is an emerging concept, and this study adds evidence that gut bacteria can influence skin inflammation through systemic immune modulation.
Questions still open
- Would these probiotics work in human rosacea patients?
- How long would the anti-inflammatory effect last?
- Is the gut-skin axis mechanism the same in humans?
Common questions
Can probiotics help rosacea?
What is LL-37's role in rosacea?
Read the original research
Probiotics suppress LL37 generated rosacea-like skin inflammation by modulating the TLR2/MyD88/NF-κB signaling pathway.
Food & function, 15(17), 8916-8934
Citation
Qi, Xinyue; Xiao, Yiran; Zhang, Xinfeng; Zhu, Zhenlin; Zhang, Hongyan; Wei, Jing; Zhao, Zhixiang; Li, Ji; Chen, Tingtao. (2024). Probiotics suppress LL37 generated rosacea-like skin inflammation by modulating the TLR2/MyD88/NF-κB signaling pathway.. Food & function, 15(17), 8916-8934. https://doi.org/10.1039/d4fo03083d