Avalos-Díaz E, Alvarado-Flores E, Herrera-Esparza R
Immunotechnology Unit, CBE, Universidad Autónoma de Zacatecas, Guadalupe, Mexico.
Rev Rhum Engl Ed. 1999 Jan;66(1):13-9.
To determine whether UV-A irradiation induces synthesis of inflammatory cytokines in the skin.
Human keratinocytes and dermal fibroblasts were cultured and exposed to various doses of UV-A radiation. The cellular distribution of IL-6 and TNF alpha was determined by indirect immunofluorescence and by flow cytometry with monoclonal anti-IL-6 and anti-TNF alpha antibodies. Cytokine production was measured in the supernatants using an ELISA. IL-6 and TNF alpha transcription induced by UV-A was determined by reverse transcriptase-polymerase chain reaction (RT-PCR) amplification.
IL-6 and TNF alpha were detected in small amounts in nonUV-A-irradiated cell. UV-A exposure was followed by significant increases in IL-6 and TNF alpha expression and by small increases in IL-6 and TNF alpha levels in culture supernatants. RT-PCR demonstrated a UV-A-mediated increase in the transcription of IL-6 and TNF alpha genes.
Synthesis of IL-6 and TNF alpha can be induced by UV-A irradiation. This effect of UV-A may contribute to the inflammatory skin changes seen during lupus flare-ups after sun exposure.
确定紫外线A（UV-A）照射是否会诱导皮肤中炎性细胞因子的合成。
培养人角质形成细胞和真皮成纤维细胞，并使其暴露于不同剂量的UV-A辐射下。使用单克隆抗白细胞介素-6（IL-6）和抗肿瘤坏死因子α（TNFα）抗体，通过间接免疫荧光法和流式细胞术确定IL-6和TNFα的细胞分布。使用酶联免疫吸附测定法（ELISA）测量上清液中的细胞因子产生量。通过逆转录聚合酶链反应（RT-PCR）扩增确定UV-A诱导的IL-6和TNFα转录。
在未接受UV-A照射的细胞中检测到少量的IL-6和TNFα。UV-A照射后，IL-6和TNFα的表达显著增加，培养上清液中IL-6和TNFα水平略有升高。RT-PCR证明UV-A介导了IL-6和TNFα基因转录的增加。
UV-A照射可诱导IL-6和TNFα的合成。UV-A的这种作用可能导致日晒后狼疮发作期间出现的皮肤炎症变化。
