Local increase in interleukin-1-like activity following UVB irradiation of human skin in vivo.

Institute of Dermatology, St Thomas' Hospital, London, United Kingdom.
Photo-dermatology 01/1990; 6(6):268-74.
Source: PubMed

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.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Cytokines induced in skin by ultraviolet radiation cause local and systemic immunosuppression. Tumor necrosis factor alpha, interleukin-1, and interleukin-10 are key mediators in the mouse, but less is known about cytokine synthesis and function in ultraviolet-irradiated human skin. We exposed human skin to 3 minimal erythema doses of solar-simulated radiation and raised suction blisters at intervals to 72 h. Alloantigen presentation was suppressed in a mixed epidermal cell-lymphocyte reaction by 69% from 4 to 15 h post-solar-simulated radiation, but recovered to control values by 24 h. Tumor necrosis factor alpha was raised at 4 h after solar-simulated radiation, reached a maximum 8-fold increase at 15 h, then rapidly declined to control values. Interleukin-1alpha and interleukin-1beta were first increased at 15 h, and remained raised to 72 h, although interleukin-1beta declined from its 15 h maximum. Interleukin-10 increased a maximum 2-fold between 15 and 24 h, coincident with recovery of mixed epidermal cell-lymphocyte reaction responses and downregulation of tumor necrosis factor alpha and interleukin-1beta. Solar-simulated radiation differentially affected soluble tumor necrosis factor alpha receptors; soluble tumor necrosis factor-RI was suppressed 33% at 8-15 h whereas soluble tumor necrosis factor-RII increased 2-fold from 15 to 48 h. Interleukin-1 receptor antagonist was raised at all times post-irradiation. Interleukin-12 was not detectable in control or irradiated skin. These kinetics suggest the tumor necrosis factor alpha network has primary importance in ultraviolet-damaged human skin. The small increase in interleukin-10 implies that 3 minimal erythema doses of solar-simulated radiation is the threshold dose for its induction and local, rather than systemic, functions for interleukin-10 in immunosuppression and regulation of other cytokines.
    Journal of Investigative Dermatology 06/1999; 112(5):692-8. DOI:10.1046/j.1523-1747.1999.00570.x · 6.37 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The effectiveness of ultraviolet (UV) radiation, visible light, or infrared light therapy for the treatment of acne is the subject of ongoing scientific debate. This study was conducted to investigate changes in sebum production and the expression of inflammatory cytokines, matrix metalloproteinases (MMPs), and antimicrobial peptides (AMPs), following exposure of cultured human sebocytes to UVA radiation and light at wavelengths of 650 nm and 830 nm. Reverse transcription polymerase chain reaction assays were performed to measure the gene expression levels of inflammatory cytokines (interleukin [IL]-1β, IL-6, IL-8, and tumor necrosis factor-α), MMPs (MMP-1, MMP-3, and MMP-9), and AMPs (psoriasin, hBD-2, hBD-3, and LL-37) in cultured sebocytes after exposure to UVA radiation (2 J/cm(2), 3 J/cm(2), and 5 J/cm(2)) and light at wavelengths of 650 nm (14 J/cm(2), 29 J/cm(2), and 87 J/cm(2)) and 830 nm (5 J/cm(2), 10 J/cm(2), and 30 J/cm(2)). Expression of inflammatory cytokine proteins and sebum production were measured using enzyme-linked immunoassays and a lipid analysis kit, respectively. Exposure of cultured sebocytes to UVA radiation and light at wavelengths of 650 nm and 830 nm did not show a significant increase in the expression of inflammatory cytokines, MMPs, or AMPs. Sebum production was not significantly decreased after exposure to UVA radiation and light at both wavelengths. We propose that UVA radiation, visible light, and infrared light can be used to target Propionibacterium acnes for the treatment of acne, without an increase in the expression of inflammatory biomarkers and sebum production.
    Annals of Dermatology 04/2015; 27(2):163-70. DOI:10.5021/ad.2015.27.2.163 · 0.95 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Ultraviolet light radiation in sunlight is known to cause major alterations in growth and differentiation patterns of exposed human tissues. The specific effects depend on the wavelengths and doses of the light, and the nature of the exposed tissue. Both growth inhibition and proliferation are observed, as well as inflammation and immune suppression. Whereas in the clinical setting, these responses may be beneficial, for example, in the treatment of psoriasis and atopic dermatitis, as an environmental toxicant, ultraviolet light can induce significant tissue damage. Thus, in the eye, ultraviolet light causes cataracts, while in the skin, it induces premature aging and the development of cancer. Although ultraviolet light can damage many tissue components including membrane phospholipids, proteins, and nucleic acids, it is now recognized that many of its cellular effects are due to alterations in growth factor- and cytokine-mediated signal transduction pathways leading to aberrant gene expression. It is generally thought that reactive oxygen intermediates are mediators of some of the damage induced by ultraviolet light. Generated when ultraviolet light is absorbed by endogenous photosensitizers in the presence of molecular oxygen, reactive oxygen intermediates and their metabolites induce damage by reacting with cellular electrophiles, some of which can directly initiate cell signaling processes. In an additional layer of complexity, ultraviolet light-damaged nucleic acids initiate signaling during the activation of repair processes. Thus, mechanisms by which solar ultraviolet radiation triggers cell signal transduction are multifactorial. The present review summarizes some of the mechanisms by which ultraviolet light alters signaling pathways as well as the genes important in the beneficial and toxic effects of ultraviolet light.
    Toxicology and Applied Pharmacology 04/2004; 195(3):288-97. DOI:10.1016/j.taap.2003.09.028 · 3.63 Impact Factor