Characterization of an interleukin 1 receptor antagonist protein released from ultraviolet-irradiated epidermal sheet

Hirao, Tetsuji; Aoki, Hiroe; Ichikawa, Hideyuki; Sato, Yoshihisa

doi:10.1016/s0923-1811(96)00572-5

Cited by 10 publications

(7 citation statements)

References 27 publications

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“…Because of the functionally competitive relationship of IL‐1Ra with IL‐1α and IL‐1β, ratios of IL‐1Ra over IL‐1α and IL‐1Ra over IL‐1β were calculated (12,26–28). Thus, we found the geometric mean of IL‐1Ra/IL‐1α in the PLE patients to drop from 1166 (423–3211; 95% CI) to 427 (195–934) and 371 (195–706) after three and six MED, respectively, and from 3020 (2187–4169) to 1023 (728–1438) and 708 (461–1087) in controls.…”

Section: Resultsmentioning

confidence: 99%

Reduced IL‐1Ra/IL‐1 ratio in ultraviolet B‐exposed skin of patients with polymorphic light eruption

Janssens

Pavel

Tensen

et al. 2009

Experimental Dermatology

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Polymorphic light eruption (PLE) is a putative delayed-type allergic reaction to (solar) ultraviolet (UV) exposure. Inadequate immune suppression after UVB-induced sunburn appears to be associated with reduced trafficking of Langerhans cells (LCs) out of and neutrophils into the epidermis of patients sensitive to UVB provocation of PLE. Therefore, we investigated whether pro-inflammatory and chemotactic cytokines are differentially expressed in UVB-irradiated skin of UVB-provocable PLE patients (n = 6) and age- and gender-matched healthy controls (n = 6). Interstitial interleukin-1alpha (IL-1alpha), IL-1beta, IL-1Ra, IL-4, IL-8, tumor necrosis factor-alpha (TNF-alpha), macrophage inflammatory protein 1-alpha (MIP-1alpha), MIP-1beta and monocyte chemotactic protein-1 (MCP-1) were measured in suction blister fluid raised 16 h after exposure to 0, three and six minimal erythemal UVB doses. In unirradiated skin, the IL-1Ra levels were significantly lower in the PLE patients than in controls (P < 0.05). IL-8 and TNF-alpha levels increased strongly upon UVB irradiation in both groups. No differential shifts in cytokine profiles were found that could explain a reduced trafficking of Langerhans cells and neutrophils in PLE patients. Dose-trend analyses showed that UVB irradiation caused significant increases in IL-1alpha in both groups, and that the levels of IL-1alpha and IL-1beta were on average twofold higher in the PLE group (P = 0.03 and P = 0.004, respectively.). Accordingly, the ratios of IL-1Ra over IL-1alpha and over IL-1beta were overall lower in the skin of PLE patients (P = 0.015 and P < 0.001, respectively.). This shift in cytokines in UVB-irradiated skin of PLE patients reveals an amplified early pro-inflammatory cytokine response, which may contribute to the allergic reaction to UVB radiation.

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Section: Resultsmentioning

confidence: 99%

Reduced IL‐1Ra/IL‐1 ratio in ultraviolet B‐exposed skin of patients with polymorphic light eruption

Janssens

Pavel

Tensen

et al. 2009

Experimental Dermatology

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“…UV-B irradiation is also known to induce the release of natural IL-1 inhibitors, epidermal cell contra-IL-1 and the endogenous IL-1 receptor antagonist (IL-1ra) in keratinocytes [54, 55]. The release of these molecules is implicated in the regulation of immune and proliferative responses by blocking IL-1 activity.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-1αInduction in Human Keratinocytes (HaCaT): AnIn VitroModel for Chemoprevention in Skin

Magcwebeba

Riedel

Swanevelder

et al. 2012

Journal of Skin Cancer

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Long-term exposure to UV irradiation and toxic chemicals is associated with chronic inflammation that contributes to skin cancer development with interleukin-1 alpha (IL-1α), constitutively produced by keratinocytes, playing a pivotal role in skin inflammation. The aim of this study was to investigate the modulation of IL-1α production in the HaCaT keratinocyte cell line. Phorbol 12-myristate 13-acetate failed to induce IL-1α in HaCaT cells, and this might be associated with the specific deficiency known to affect downstream signalling of the MEK/ERK pathway in these cells. The calcium ionophore, ionomycin, slightly enhanced the production of intracellular (icIL-1α), but this resulted in a necrotic release at higher concentrations. UV-B exposure significantly increased the production of icIL-1α in a dose-dependent manner with a maximal induction exhibited at 24 h with minimal necrotic and apoptotic effects. Validation of the HaCaT cell model indicated that the nonsteroidal anti-inflammatory drug (NSAID), ibuprofen, and the glucocorticoid, dexamethasone, inhibited icIL-1α production, and this was associated with a slight inhibition of cell viability. The UV-B-induced keratinocyte cell model provides anin vitrosystem that could, apart from phorbol ester-like compounds, be utilised as a screening assay in identifying skin irritants and/or therapeutic topical agents via the modulation of IL-1α production.

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“…In the previous study using tape-stripped SC samples obtained from healthy volunteers, it has been shown that a single exposure of the healthy donor skin to UVB irradiation resulted in an elevation of the ratio of IL-1ra to IL-1a (19). IL-1ra was also detected in the culture supernatant of mouse epidermal sheet which had been irradiated with UVB either in vitro or in vivo (20). From this UV influence on IL-1ra production, in the present study we have investigated whether there is a regional difference in the ratio of IL-1ra to IL-1a among the face, trunk, and extremities excluding the hands and feet.…”

Section: Introductionmentioning

confidence: 97%

An increased ratio of interleukin‐1 receptor antagonist to interleukin‐1α in inflammatory skin diseases

Terada

Hirao²,

Sato³

et al. 1998

Experimental Dermatology

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IL-1 receptor antagonist (IL-1ra) is a cytokine that competitively binds the IL-1 receptor to antagonize IL-1 activity without any agonist function. Previous experiments indicated that the ratio of IL-1ra to IL-1alpha in the normal stratum corneum (SC) was much higher in the sun-exposed face than in the sun-protected area, upper arms. It was also reported by another laboratory that IL-1ra is increased in the lesional skin of psoriatic patients. This study was designed to measure the contents of IL-1alpha and IL-1ra in non-lesional and pathological SC obtained from inflammatory skin diseases including psoriasis and non-psoriatic dermatoses such as atopic dermatitis. The SC materials were obtained with a non-invasive tape-stripping method. Their soluble fractions were prepared and assayed for IL-1alpha and IL-1ra by enzyme-linked immunosorbent assays. As a result we confirmed the previous findings that the ratio of IL-1ra to IL-1alpha in the normal SC was much higher in the face than in the sun-protected sites, the trunk as well as extremities. Next, we found that IL-1alpha contents were significantly reduced in the SC samples obtained from inflammatory skin regardless of whether their IL-1ra contents increased or unchanged. Moreover, we noted that an increased ratio of IL-1ra to IL-1alpha in the SC was not specific to psoriasis, but was also found in other inflammatory skin diseases including atopic dermatitis. This ratio was found to become lower after successful treatment of these skin lesions with topical glucocorticoids. We conclude from these observations that the increased ratio of IL-1ra to IL-1alpha in the SC is a non-specific phenomenon that can occur in any inflammatory skin diseases regardless of the inflammatory pattern, probably reflecting a skin regulation process against various kinds of inflammation.

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Characterization of an interleukin 1 receptor antagonist protein released from ultraviolet-irradiated epidermal sheet

Cited by 10 publications

References 27 publications

Reduced IL‐1Ra/IL‐1 ratio in ultraviolet B‐exposed skin of patients with polymorphic light eruption

Reduced IL‐1Ra/IL‐1 ratio in ultraviolet B‐exposed skin of patients with polymorphic light eruption

Interleukin-1αInduction in Human Keratinocytes (HaCaT): AnIn VitroModel for Chemoprevention in Skin

An increased ratio of interleukin‐1 receptor antagonist to interleukin‐1α in inflammatory skin diseases

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