The precise contribution of the commensal bacterium Propionibacterium acnes (P. acnes) in the inflammatory response associated with acne vulgaris remains controversial. In this issue Qin et al. show that P. acnes induces robust IL-1β secretion in monocytic cells by triggering the activation of the NLRP3 inflammasome. In vivo, the encounter of P. acnes and macrophages in the peri-follicular dermis could locally result in the release of substantial amounts of IL-1β and therefore exacerbate inflammation. Such findings suggest that molecules targeting IL-1β and/or the NLRP3 inflammasome may constitute new treatment possibilities for acne vulgaris.