SKIN and associated MICROBIOTA together build a complex community that describes an evolutionary organ under genetic and evolutionary control enabling the protection against exposome. This community has a strong symbiotic relationship in a continuous cross-talk, which influences both counterparts’ behaviour. However the knowledge of skin biology and aging process has been built up during decades without consideration of the interactions with associated microbiota community. The scientific community is now facing a lack of knowledge in this respect and also the challenge in re-thinking the fundamentals of the skin ageing process.
Age-associated low-grade inflammation (inflammaging) is now recognised as being a driving force of many age-associated diseases linked to irreversible cellular and molecular damage that is not clinically evident because it slowly accumulates over decades. Inflammaging is believed to be a consequence of a re-modelling of the innate and acquired immune system, resulting both in cumulative lifetime exposure to pro-inflammatory cytokines at older ages and production of reactive oxygen determining modification to skin appearance and involvement in chronic diseases. (Baylis et al. Longevity & Healthspan 2013 2:8).
The presentation will focus on the effects of UV induced inflammasome in the aging process in presence/absence of bacteria representative of 2 main classes: commensal ( S.epidermidis ATCC 1228 and C.acnes ATCC 11828) and opportunistic ( S.aureus ATCC 33591 and C.acnes virulent ATCC 1182). Reconstructed Living 3D Human Skin was used that mimics the real site where the skin-microbiome interaction occurs and allows the identification of the mechanism by which the bacteria can influence skin health and appearance and consequently the skin ageing process.
Inflammasome (oxidative stress and inflammation) has been induced by low, biologically relevant UV dose, 2MED and a dynamic approach based on inflammasome biomarkers kinetic has been applied by adopting a multiple end-points approach and targeting extracellular matrix proteins (pro-collagens, pro-elastin, integrins) at the dermal level.
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