Abstract
Reactive oxygen species (ROS) can be both beneficial and deleterious. Under normal physiological conditions, ROS production is tightly regulated, and ROS participate in both pathogen defense and cellular signaling. However, insufficient ROS detoxification or ROS overproduction generates oxidative stress, resulting in cellular damage. Oxidative stress has been linked to various inflammatory diseases. Inflammation is an essential response in the protection against injurious insults and thus important at the onset of wound healing. However, hampered resolution of inflammation can result in a chronic, exaggerated response with additional tissue damage. In the pathogenesis of several inflammatory skin conditions, e.g., sunburn and psoriasis, inflammatory-mediated tissue damage is central. The prolonged release of excess ROS in the skin can aggravate inflammatory injury and promote chronic inflammation. The cellular redox balance is therefore tightly regulated by several (enzymatic) antioxidants and pro-oxidants; however, in case of chronic inflammation, the antioxidant system may be depleted, and prolonged oxidative stress occurs. Due to the central role of ROS in inflammatory pathologies, restoring the redox balance forms an innovative therapeutic target in the development of new strategies for treating inflammatory skin conditions. Nevertheless, the clinical use of antioxidant-related therapies is still in its infancy.
Highlights
The primary function of healthy skin is to form a physical and chemical barrier between the external environment and the organism’s internal milieu to defend against injurious insults
The strength and duration of the inflammatory response depends on stimulus and context, and the initial steps are stereotyped as part of the innate immune response [1]
Reactive oxygen species (ROS) are free radicals generated from molecular oxygen, such as superoxide anion (O2−), hydroxyl radical (HO), and non-radical species including hydrogen peroxide (H2O2)
Summary
The primary function of healthy skin is to form a physical and chemical barrier between the external environment and the organism’s internal milieu to defend against injurious insults. Pathogen-mediated activation of the inflammasome induces a specific form of caspase-1-dependent cell death, pyroptosis, that results in osmotic swelling and plasma membrane rupture [10,11] This induces a strong inflammatory response via the release of pro-inflammatory cytokines and spreading of pro-inflammatory molecules [12]. In contrast to immune cells, human keratinocytes constitutively express inflammasome proteins and are a potent source of the pro-inflammatory cytokines pro-IL1α and pro-IL1β [13,14,15], which are activated and released upon UV exposure [13,16]. The prolonged presence of oxidative stress is postulated to promote and fuel these deleterious inflammatory processes and may form a novel target for treatment of chronic inflammatory conditions
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