SKIN INFLAMMAGING


Skin inflammaging and the role of Ectoin


Disha Patel and Eva Galik - Bitop


Inflammaging, coined by Franceschi et al in 2000, refers to the chronic, low-grade inflammation that increases with age and contributes to age-related diseases. The World Health Organization’s 2015 World Report on Aging and Health highlighted the need for healthy ageing strategies, recognizing skin health as a key yet underappreciated factor. Skin constantly faces external and internal


stressors—UV radiation, pollution, and microbes—that drive persistent inflammation. This leads to visible ageing signs like wrinkles, rough texture, reduced regeneration, and weakened barrier function. This article examines key inflammaging mechanisms, including mitochondrial dysfunction, ROS, inflammasome activation, cytokines (IL-1, IL-6, IL-8, TNF-α), MMPs, and SASP. Bitop Ectoin® natural is demonstrated to deliver therapeutic efficacy across major inflammaging mechanisms, establishing its role in next-generation skin longevity solutions. Ectoin reduces pro-inflammatory cytokine


expression, inhibits oxidative stress, and protects cellular structures through its unique hydro-complex mechanism. Clinical studies show significant improvements in skin hydration, barrier repair, and reduced inflammatory markers, establishing Ectoin as a gold-standard active for prevention, treatment, and repair of inflammaging.


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Characteristics of skin inflammaging The five states of skin inflammaging are as follows: low-grade, controlled, asymptomatic, chronic, and systemic.2


These response events


are characterized by interactions between the cells and factors in the microenvironment and by regulation of the balance between physiological and pathological signaling networks.


In common conditions, inflammatory


responses disappear when proinflammatory factors in infection and tissue injuries are eliminated and then change into a highly active and well-regulated balanced state, which is called resolving inflammation.3


Cellular and molecular interactions Inflammaging is sustained through a complex interplay between innate and adaptive immune components, including macrophages, neutrophils, T cells, and cytokine networks. Homeostasis is maintained through feedback loops that limit excessive immune activation and promote tissue repair. Disruption of these mechanisms can lead to


maladaptive signaling, resulting in a transition from controlled, asymptomatic inflammation to chronic, systemic inflammation that contributes to age-related pathologies. As the largest organ of the body, skin is


continuously exposed to external stressors such as UV radiation, pollutants as well as air particulate matter and human microbiome. The process of inflammaging involves mechanisms of accumulation of senescence cells in different compartments of the skin based on cell types and their association with skin resident immune cells to describe changes in cutaneous immunity during the ageing process.10 As global life expectancy continues to rise,


Figure 1: Schematic network connecting senescence/immunosenescence, inflammaging, frailty, and age-related diseases


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we are challenged with maintaining health into old age. One strategy is to target the chronic


November 2025 PERSONAL CARE


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