INTRODUCTION
As humans continue to live longer, there is an increased interest in research on age-related physiologic changes and illnesses. This study of aging and its link to age-related chronic conditions has given rise to a new research field called geroscience. Geroscientists assume that the mechanisms that drive aging and those that drive age-related diseases largely overlap.Thinking along these lines, in 2000, Claudio Franceschi developed the concept of “inflammaging,†driving researchers to recognize that aging is a complex and multifaceted phenomenon that demands a holistic view of the body’s physiology.1-3 Franceschi initially described inflammaging as an extension on the network theory of aging; he proposed that a reduction in the ability to cope with stressors, coupled with a progressive increase in proinflammatory status was the cause of inflammaging.4 He proposed that aging is associated with a chronic, sterile, low-grade inflammation called inflammaging.5
It is important to distinguish between inflammaging and acute, transient inflammation. Transient inflammation in the face of tissue injury or invading pathogens is beneficial as a defensive immune response, but when individuals have persistently elevated levels of inflammation, that process is considered inflammaging, and thus detrimental. Inflammaging is thought to contribute to many age-related chronic diseases including cardiovascular disease, diabetes, Alzheimer’s disease, and certain cancers. A number of other studies have looked at the role of proinflammatory cytokines and found that IL-6 and CRP – two common markers of inflammaging – were strong predictors of physical and cognitive performance. In addition, these markers were strong predictors of mortality in the elderly population.6-10
Recent advancements in geroscience have come to conclude that inflammaging does not exist in isolation; instead, a plethora of studies have linked inflammaging with immunosenescence as a contributing factor. Immunosenescence is a collection of age-related changes in the adaptive immune system. Immunosenescence refers to the concept that the adaptive immune system (ie, B cells and T cells) becomes less effective with age and the innate immune system (ie, neutrophils, macrophages, natural killer cells) becomes more dominant.11-14 Other key factors thought to contribute to inflammaging include microbiome dysbiosis and oxidative stress.15-17 This is of particular importance to dermatologists given that the skin is home to a large portion of the human microbiome and plays a key role in the prevention of oxidative stress due to biological or environmental agents.18 As such, it follows that our body’s largest organ, the skin, may be responsible for a larger role in promoting or preventing inflammaging.
In this review article, we present common dermatological diseases through the lens of inflammaging, look at how our skin may play a central role in reducing inflammaging, and highlight the need for further focused research in this area. Management of the human microbiome in the skin may even have an impact on chronic disease.
It is important to distinguish between inflammaging and acute, transient inflammation. Transient inflammation in the face of tissue injury or invading pathogens is beneficial as a defensive immune response, but when individuals have persistently elevated levels of inflammation, that process is considered inflammaging, and thus detrimental. Inflammaging is thought to contribute to many age-related chronic diseases including cardiovascular disease, diabetes, Alzheimer’s disease, and certain cancers. A number of other studies have looked at the role of proinflammatory cytokines and found that IL-6 and CRP – two common markers of inflammaging – were strong predictors of physical and cognitive performance. In addition, these markers were strong predictors of mortality in the elderly population.6-10
Recent advancements in geroscience have come to conclude that inflammaging does not exist in isolation; instead, a plethora of studies have linked inflammaging with immunosenescence as a contributing factor. Immunosenescence is a collection of age-related changes in the adaptive immune system. Immunosenescence refers to the concept that the adaptive immune system (ie, B cells and T cells) becomes less effective with age and the innate immune system (ie, neutrophils, macrophages, natural killer cells) becomes more dominant.11-14 Other key factors thought to contribute to inflammaging include microbiome dysbiosis and oxidative stress.15-17 This is of particular importance to dermatologists given that the skin is home to a large portion of the human microbiome and plays a key role in the prevention of oxidative stress due to biological or environmental agents.18 As such, it follows that our body’s largest organ, the skin, may be responsible for a larger role in promoting or preventing inflammaging.
In this review article, we present common dermatological diseases through the lens of inflammaging, look at how our skin may play a central role in reducing inflammaging, and highlight the need for further focused research in this area. Management of the human microbiome in the skin may even have an impact on chronic disease.
