Skin Immunosenescence and Type 2 Inflammation: A Mini-Review With an Inflammaging Perspective

Chen, Bangtao; Yang, Jing; Song, Yao; Zhang, Daojun; Fei, Hao

doi:10.3389/fcell.2022.835675

Cited by 17 publications

(24 citation statements)

References 92 publications

(102 reference statements)

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“…During chronological aging, the body undergoes a continuous increase in systemic low-grade inflammation, a process known as ″inflammaging″ [ 209 , 210 ]. Such chronic aging-related inflammatory response is marked by an increase in systemic levels of IL1, IL6, and IL33, as well as TNF, IFNγ, and GM-CSF [ 211 , 212 ]. The relationship between the senescence of skin-resident immune cells and inflammaging has not been fully understood yet.…”

Section: The Role Of Oxidative Stress In Chronological Senescence Of ...mentioning

confidence: 99%

“…In aged skin, decreased self-renewal capacity of in situ Langerhans cell progenitors causes a reduced number of their mature counterparts. Additionally, the lower migration propensity of these cells in geriatric individuals contributes to impaired skin barrier integrity [ 212 , 213 ]. In addition, Langerhans cells in aged skin express a low amount of human beta-defensin-3, which is an important antimicrobial peptide produced in response to microbial infection or skin dysbiosis [ 214 ].…”

Section: The Role Of Oxidative Stress In Chronological Senescence Of ...mentioning

confidence: 99%

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Focus on the Contribution of Oxidative Stress in Skin Aging

et al. 2022

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Skin aging is one of the most evident signs of human aging. Modification of the skin during the life span is characterized by fine lines and wrinkling, loss of elasticity and volume, laxity, rough-textured appearance, and pallor. In contrast, photoaged skin is associated with uneven pigmentation (age spot) and is markedly wrinkled. At the cellular and molecular level, it consists of multiple interconnected processes based on biochemical reactions, genetic programs, and occurrence of external stimulation. The principal cellular perturbation in the skin driving senescence is the alteration of oxidative balance. In chronological aging, reactive oxygen species (ROS) are produced mainly through cellular oxidative metabolism during adenosine triphosphate (ATP) generation from glucose and mitochondrial dysfunction, whereas in extrinsic aging, loss of redox equilibrium is caused by environmental factors, such as ultraviolet radiation, pollution, cigarette smoking, and inadequate nutrition. During the aging process, oxidative stress is attributed to both augmented ROS production and reduced levels of enzymatic and non-enzymatic protectors. Apart from the evident appearance of structural change, throughout aging, the skin gradually loses its natural functional characteristics and regenerative potential. With aging, the skin immune system also undergoes functional senescence manifested as a reduced ability to counteract infections and augmented frequency of autoimmune and neoplastic diseases. This review proposes an update on the role of oxidative stress in the appearance of the clinical manifestation of skin aging, as well as of the molecular mechanisms that underline this natural phenomenon sometimes accelerated by external factors.

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Section: The Role Of Oxidative Stress In Chronological Senescence Of ...mentioning

confidence: 99%

Section: The Role Of Oxidative Stress In Chronological Senescence Of ...mentioning

confidence: 99%

Focus on the Contribution of Oxidative Stress in Skin Aging

et al. 2022

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“…Beyond other cell types, skin fibroblasts are the main cell type present in skin connective tissue (dermis), presenting a crucial role as effector cells executing physiologic tissue repair, and pathological fibrogenesis leading to chronic fibrosing conditions in certain circumstances [ 2 ]. Skin fibroblasts also participate in the immune response of the skin, mainly releasing cytokines and growth factors [ 3 ]. During senescence, aging-induced immunosenescence predisposes inflammatory disturbances of the skin, including pruritic dermatoses and type 2 inflammation [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

“…Skin fibroblasts also participate in the immune response of the skin, mainly releasing cytokines and growth factors [ 3 ]. During senescence, aging-induced immunosenescence predisposes inflammatory disturbances of the skin, including pruritic dermatoses and type 2 inflammation [ 3 ]. This immunosenescence is characterized by a chronic release of pro-inflammatory cytokines driving type 2 inflammatory dermatoses [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

“…During senescence, aging-induced immunosenescence predisposes inflammatory disturbances of the skin, including pruritic dermatoses and type 2 inflammation [ 3 ]. This immunosenescence is characterized by a chronic release of pro-inflammatory cytokines driving type 2 inflammatory dermatoses [ 3 ]. Therefore, scientists around the world are looking for strategies that are capable of preventing skin infections, especially in immunocompromised individuals [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

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Hydrolyzed Collagen Induces an Anti-Inflammatory Response That Induces Proliferation of Skin Fibroblast and Keratinocytes

Brandão-Rangel

Oliveira²,

Olimpio³

et al. 2022

Nutrients

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Collagen-based products are found in different pharmaceuticals, medicine, food, and cosmetics products for a wide variety of applications. However, its use to prevent or improve the health of skin is growing dizzyingly. Therefore, this study investigated whether collagen peptides could induce fibroblast and keratinocyte proliferation and activation beyond reducing an inflammatory response induced by lipopolysaccharide (LPS). Human skin fibroblasts (CCD-1072Sk) and human keratinocytes (hKT-nh-skp-KT0026) were seeded at a concentration of 5 × 104 cells/mL. LPS (10 ng/mL) and three doses of collagen peptides (2.5 mg/mL, 5 mg/mL, 10 mg/mL) were used. The readout parameters were cell proliferation; expression of inducible nitric oxide synthase (iNOS); expression of pro-collagen-1α by fibroblasts; and secretion of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor α (TNF-α), transforming growth factor β (TGF-β), and vascular endothelial growth factor (VEGF) by both cell types. The results demonstrated that all doses of collagen supplementation induced increased proliferation of both human fibroblasts (p < 0.01) and human keratinocytes (p < 0.001), while only the dose of 10 mg/mL induced an increased expression of pro-collagen-1α by fibroblasts. Similarly, only the dose of 10 mg/mL reduced LPS-induced iNOS expression in fibroblasts (p < 0.05) and keratinocytes (p < 0.01). In addition, collagen supplementation reduced the LPS-induced IL-1β (p < 0.05), IL-6 (p < 0.001), IL-8 (p < 0.01), and TNF-α (p < 0.05), and increased the TGF-β and VEGF expression in fibroblasts. Furthermore, collagen supplementation reduced the LPS-induced IL-1β (p < 0.01), IL-6 (p < 0.01), IL-8 (p < 0.01), and TNF-α (p < 0.001), and increased the TGF-β (p < 0.05) and VEGF (p < 0.05) expression in keratinocytes. In conclusion, collagen peptides were found to induce fibroblast and keratinocyte proliferation and pro-collagen-1α expression, involving increased expression of TGF-β and VEGF, as well as the suppression of an inflammatory response induced by LPS.

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