Local increase in interleukin-1-like activity following UVB irradiation of human skin in vivo.
ABSTRACT Using an in vivo skin chamber method, we demonstrated increased release of interleukin-1 (IL-1)-like activity at the site of irradiation with 3 times the minimal erythema dose of ultraviolet B (UVB). IL-1-like activity was estimated using the mouse thymocyte amplification assay. UVB-augmented release of IL-1-like activity peaked 1 h after irradiation and levels returned to baseline by 2 h. Release of IL-1-like activity from human skin after exposure to UV radiation may account for some of the local and systemic features of the sunburn response.
SourceAvailable from: Miroslav Blumenberg[Show abstract] [Hide abstract]
ABSTRACT: In wound healing and many pathologic conditions, keratinocytes become activated: they turn into migratory, hyperproliferative cells that produce and secrete extracellular matrix components and signaling polypeptides. At the same time, their cytoskeleton is also altered by the production of specific keratin proteins. These changes are orchestrated by growth factors, chemokines, and cytokines produced by keratinocytes and other cutaneous cell types. The responding intracellular signaling pathways activate transcription factors that regulate expression of keratin genes. Analysis of these processes led us to propose the existence of a keratinocyte activation cycle, in which the cells first become activated by the release of IL-1. Subsequently, they maintain the activated state by autocrine production of proinflammatory and proliferative signals. Keratins K6 and K16 are markers of the active state. Signals from the lymphocytes, in the form of Interferon-, induce the expression of K17 and make keratinocytes contractile. This enables the keratinocytes to shrink the provisional fibronectin-rich basement membrane. Signals from the fibroblasts, in the form of TGF-, induce the expression of K5 and K14, revert the keratinocytes to the healthy basal phenotype, and thus complete the activation cycle.Abbreviations: ERK, extracellularly regulated kinase; IKK, IkB kinase; IRAK, IL-1 receptor associated kinase; JAK, Janus activated kinase; MAPK, mitogen activated protein kinase; MEK, MAPK/ERK kinase; NIK, NFkB inducing kinase; PKC, protein kinase-C; TAK, TRAF associated kinase; TRADD, TNF receptor associated death domain; TRAF, TNF receptor associated factorJournal of Investigative Dermatology 04/2001; 116(5):633-640. DOI:10.1046/j.1523-1747.2001.01327.x · 6.37 Impact Factor
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ABSTRACT: Sebaceous gland hyperplasia and increased sebum secretion after irradiation of ultraviolet (UV)-B has been widely accepted. This study was performed to clarify expression of inflammatory cytokines after irradiating UV-B in cultured sebocytes. Reverse transcription polymerase chain reaction was performed to measure gene expression of inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8 and tumor necrosis factor-α, in cultured sebocytes after exposure to 40 and 70 mJ/cm(2) UV-B. Protein expression of inflammatory cytokines and lipid production in cultured sebocytes after exposure to UV-B were measured using enzyme-linked immunoassay and lipid analysis kit. The expression of inflammatory cytokines, especially IL-1β and IL-8, was significantly increased in cultured sebocytes after treatment with UV-B. Many more studies on the effect of UV-B on sebaceous glands should be performed to reveal the pathogenic mechanism of acne.The Journal of Dermatology 12/2013; 40(12). DOI:10.1111/1346-8138.12330 · 2.35 Impact Factor
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ABSTRACT: To understand the expressions and transduction pathways of cytokines in ultraviolet (UV)A-irradiated keratinocytes. We cultured human keratinocytes of the HaCaT cell line and investigated both mRNA and protein expressions of cytokines in cells that were not irradiated or were exposed to 2.4 J/cm(2) UVA, with or without an antioxidant (beta-carotene) or a c-Jun N-terminal kinase (JNK) inhibitor (SP600125). We demonstrated that the expression levels of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta were up-regulated in irradiated cells. IL-10 was not detected in non-irradiated cells, but was observed in irradiated cells. JNK was activated in irradiated cells and this could be antagonized by beta-carotene. The UVA-induced up-regulation of these cytokines was also antagonized by beta-carotene. SP600125 inhibited the UVA-induced increase in the expression of TNF-alpha mRNA and protein and in the expression of IL-1beta mRNA. The results suggest that oxidative stress may be an early intermediate effect in JNK-dependent UVA induction of cytokine expression in human keratinocytes in vitro.Photodermatology Photoimmunology and Photomedicine 02/2010; 26(1):28-35. DOI:10.1111/j.1600-0781.2009.00481.x · 1.52 Impact Factor