McGlade J P, Gorman S, Zosky G R, Larcombe A N, Sly P D, Finlay-Jones J J, Turner D J, Hart P H
Telethon Institute for Child Health Research and Centre for Child Health Research, University of Western Australia, Perth, WA, Australia.
Clin Exp Allergy. 2007 Sep;37(9):1267-76. doi: 10.1111/j.1365-2222.2007.02750.x.
Over recent decades, there has been a significant global increase in the prevalence of asthma, an inflammatory disease of the respiratory system. While ultraviolet radiation (UV) has been used successfully in the treatment of inflammatory conditions such as psoriasis, studies of UV-induced regulation of allergic respiratory responses have been rare, and have not analysed in vivo measurements of airway hyperresponsiveness (AHR) or the antigen specificity of the UV-induced effects.
To investigate the regulatory properties of erythemal ultraviolet B (UVB) irradiation of the skin and the induction of allergen-induced airway immunity in a murine asthma model, and to examine the mechanisms involved.
BALB/c mice were exposed to a single erythemal dose of UV 3 days before intraperitonial sensitization (day 0) and boost (day 14) with the antigen, ovalbumin (OVA). Airway-associated, asthma-like responses to aerosolized OVA at day 21 were analysed including (a) AHR measured in vivo, (b) OVA-specific proliferative responses and cytokine production by cells from the lung-draining lymph nodes (LDLN), and (c) inflammatory cells and cytokines in the bronchoalveolar lavage fluid. To determine UVB-induced mechanisms of regulation, LDLN cells from UVB irradiated, OVA-sensitized mice were adoptively transferred into naïve BALB/c mice that were subsequently sensitized and challenged with OVA, or a non-specific antigen.
UVB irradiation of skin significantly suppressed AHR to methacholine and OVA-specific responses in the LDLN and in the lung compartment. Reduced OVA-specific responses by LDLN cells from both UVB irradiated mice and mice that received 5 x 10(6) LDLN cells from UVB irradiated, but not from non-irradiated, OVA-sensitized mice suggested that UVB-induced regulatory cells are responsible for many of the asthma-reducing effects of dorsal UVB exposure.
UVB irradiation of skin suppresses AHR and cellular responses of the airways to respiratory allergens. Further, this study implicates UVB or its downstream mediators as a potential approach to reducing the severity of asthma.
在最近几十年里，作为一种呼吸系统炎症性疾病，哮喘在全球的患病率显著上升。虽然紫外线辐射（UV）已成功用于治疗诸如银屑病等炎症性疾病，但关于紫外线诱导调节过敏性呼吸道反应的研究却很少，且尚未分析气道高反应性（AHR）的体内测量结果或紫外线诱导效应的抗原特异性。
在小鼠哮喘模型中研究皮肤红斑性紫外线B（UVB）照射的调节特性以及变应原诱导的气道免疫的诱导情况，并探讨其中涉及的机制。
在腹腔致敏（第0天）和用抗原卵清蛋白（OVA）加强免疫（第14天）前3天，对BALB/c小鼠进行单次红斑剂量的紫外线照射。分析第21天时对雾化OVA的气道相关哮喘样反应，包括：（a）体内测量的AHR；（b）OVA特异性增殖反应以及肺引流淋巴结（LDLN）细胞产生的细胞因子；（c）支气管肺泡灌洗液中的炎性细胞和细胞因子。为了确定UVB诱导的调节机制，将来自经UVB照射、OVA致敏小鼠的LDLN细胞过继转移到未致敏的BALB/c小鼠中，随后这些小鼠用OVA或非特异性抗原进行致敏和激发。
皮肤UVB照射显著抑制了对乙酰甲胆碱的AHR以及LDLN和肺区的OVA特异性反应。来自经UVB照射小鼠以及接受了5×10⁶个来自经UVB照射而非未照射的OVA致敏小鼠的LDLN细胞的小鼠，其LDLN细胞的OVA特异性反应降低，这表明UVB诱导的调节细胞是背部UVB照射减轻哮喘作用的主要原因。
皮肤UVB照射可抑制AHR以及气道对呼吸道变应原的细胞反应。此外，本研究表明UVB或其下游介质是减轻哮喘严重程度的一种潜在方法。
