Probiotics suppress LL37 generated rosacea-like skin inflammation by modulating the TLR2/MyD88/NF-κB signaling pathway.

Rosacea, a chronic inflammatory dermatological condition, is characterized by facial erythema and pustules. Recent investigations have delved into the interplay between the gut microbiota and rosacea pathogenesis, unveiling promising avenues for therapeutic intervention. In this study, we screened and isolated strains23-006 and23-008 from the feces of healthy volunteers and evaluated the intervention effects of probiotics on rosacea by constructing an LL37 induced rosacea-like mouse model. Our results showed that both23-006 and23-008 were probiotic strains with favourable properties. In specific, we observed that both23-006 and23-008 alleviated skin lesions, reduced skin inflammatory infiltrates, and decreased the expression of inflammatory factors in mice, with the combination of23-006 and23-008 having the most significant effect. Moreover, the combination of strains reduced the expression of cathelicidin LL37 and rosacea-associated factors by inhibiting the TLR2/MyD88/NF-κB pathway. The 16S rRNA analysis showed that the combination enhanced the intestinal barrier, restored intestinal microbiota homeostasis, and up-regulated the abundance ofwhile down-regulating the abundance ofand. We also explored the effects of postbiotics of23-006 and23-008 on rosacea. While postbiotics could also ameliorate the rosacea-like phenotype in micethe TLR2/MyD88/NF-κB pathway, the effects were not as pronounced as those observed with probiotic treatment. However, the postbiotics still enhanced the intestinal barrier, up-regulated theabundance, and modulated the intestinal microbiota. In conclusion, our study revealed that23-006 and23-008 improved rosacea by regulating the TLR2/MyD88/NF-κB pathway and intestinal microbiota, providing a theoretical basis for the treatment of rosacea.