Antibodies Elicited by Inactivated Propionibacterium acnes-Based Vaccines Exert Protective Immunity and Attenuate the IL-8 Production in Human Sebocytes: Relevance to Therapy for Acne Vulgaris

Abstract

Propionibacterium acnes is a key pathogen involved in the progression of inflammation in acne vulgaris. We examined whether vaccination against P. acnes suppressed P. acnes-induced skin inflammation. Inactivation of P. acnes with heat was employed to create a P. acnes-based vaccine. Intranasal immunization in mice with this inactivated vaccine provoked specific antibodies against P. acnes. Most notably, immunization with inactivated vaccines generated in vivo protective immunity against P. acnes challenge and facilitated the resolution of ear inflammation in mice. In addition, antibodies elicited by inactivated vaccines effectively neutralized the cytotoxicity of P. acnes and attenuated the production of proinflammatory cytokine IL-8 in human sebocyte SZ95 cells. Intranasal immunization using heat-inactivated P. acnes-based vaccines provided a simple modality to develop acne vaccines. These observations highlight the concept that development of vaccines targeting microbial products may represent an alternative strategy to conventional antibiotic therapy.

Nicotinamide inhibits Propionibacterium acnes-induced IL-8 production in keratinocytes through the NF-κB and MAPK pathways

“…It has recently been shown that the antibodies elicited by inactivated P. acnes in intranasally immunized mice decrease IL-8 production, thereby decreasing inflammation and improving clinical signs [32]. We therefore hypothesized that the antiinflammatory effects of nicotinamide might be at least partly due to the ability of this molecule to regulate IL-8 production in our model based on keratinocytes stimulated by P. acnes.…”

An environmental contaminant, benzo(a)pyrene, induces oxidative stress-mediated interleukin-8 production in human keratinocytes via the aryl hydrocarbon receptor signaling pathway

“…The pathogenetic role of IL-8 has been postulated, at least in part, in neutrophil-related skin diseases such as psoriasis [49,50], palmoplantar pustulosis [50] and acne [48,51,52]. Propionibacterium acnes is feasible for inducing IL-8 production in various cell types including NHEKs [52,53].…”

“…IL-8 is one of the major cyto/chemokines in inflammatory response and activates the recruitment and function of neutrophils [48]. The pathogenetic role of IL-8 has been postulated, at least in part, in neutrophil-related skin diseases such as psoriasis [49,50], palmoplantar pustulosis [50] and acne [48,51,52].…”

KdPT, a Tripeptide Derivative of α-Melanocyte–Stimulating Hormone, Suppresses IL-1β–Mediated Cytokine Expression and Signaling in Human Sebocytes

“…The pathogenesis of this disease is complex, involving sebaceous gland hypertrophy, increased seborrhea with the presence of oxidized lipids, pilosebaceous duct hyperkeratinization, and colonization with Propionibacterium acnes, resulting in perifollicular inflammation (2,3). Among various mediators orchestrating the inflammatory response of the pilosebaceous unit in acne, several cytokines, including IL-1, IL-6, IL-8, and TNF-a, have been implicated (4)(5)(6)(7)(8). In particular, IL-1 appears to play a key role in the pathogenesis of acne.…”