Adipose-derived stem cells attenuate acne-related inflammation via suppression of NLRP3 inflammasome

Background: Acne is a chronic facial disease caused by Propionibacterium acnes, which proliferates within sebum-blocked skin follicles and increases inflammatory cytokine production. Several therapeutic drugs and products have been proposed to treat acne, yet no single treatment that ensures long-term treatment efficacy for all patients is available. Here, we explored the use of facial autologous fat transplant of adipose-derived stem cells (ADSCs) to dramatically reduce acne lesions. Methods: THP-1 cells were treated with active P. acnes for 24 h at different multiplicities of infection, and alterations in inflammatory factors were detected. To study the effect of THP-1 on inflammasome-related proteins, we first co-cultured ADSCs with THP-1 cells treated with P. acnes and evaluated the levels of these proteins in the supernatant. Further, an acne mouse model injected with ADSCs was used to assess inflammatory changes. Results: Propionibacterium acnes-mediated stimulation of THP-1 cells had a direct correlation with the expression of active caspase-1 and interleukin (IL)-1 beta in an infection-dependent manner. ADSCs significantly reduced the production of IL-1 beta induced by P. acnes stimulation through the reactive oxygen species (ROS)/Nod-like receptor family pyrin domain-containing 3 (NLRP3)/caspase-1 pathway. The results showed that ADSCs inhibit the skin inflammation induced by P. acnes by blocking the NLRP3 inflammasome via reducing the secretion of IL-1 beta in vivo. Conclusions: Our findings suggest that ADSCs can alter IL-1 beta secretion by restricting the production of mitochondria ROS, thereby inhibiting the NLRP3/caspase-1 pathway in P. acnes-induced inflammatory responses. This study indicates that anti-acne therapy can potentially be developed by targeting the NLRP3 inflammasome.

Automated summary

This study found that adipose-derived stem cells (ADSCs) can inhibit skin inflammation induced by Propionibacterium acnes by blocking the NLRP3 inflammasome and reducing the secretion of IL-1 beta.