Seeliger Stephan, Derian Cllaudia K, Vergnolle Nathalie, Bunnett Nigel W, Nawroth Roman, Schmelz Martin, Von Der Weid Pierre-Yves, Buddenkotte Jörg, Sunderkötter Cord, Metze Dieter, Andrade-Gordon Patricia, Harms Erik, Vestweber Dietmar, Luger Thomas A, Steinhoff Martin
Department of Pediatrics, University of Münster, Münster, Germany.
FASEB J. 2003 Oct;17(13):1871-85. doi: 10.1096/fj.02-1112com.
Proteinase-activated receptor-2 belongs to a new subfamily of G-protein-coupled receptors. Its precise role during inflammation and the underlying mechanisms is still unclear. Our study establishes that PAR-2 plays a direct proinflammatory role during cutaneous inflammation in mice and humans in vivo. In a model of experimentally induced allergic (ACD) and toxic (ICD) contact dermatitis (CD) we show that ear swelling responses, plasma extravasation, and leucocyte adherence were significantly attenuated in PAR-2 null mutant (PAR-2-/-) mice compared with wild-type (PAR-2+/+) mice, especially at early stages. The proinflammatory effects by PAR-2 activation were significantly diminished using nitric oxide-synthase inhibitors, while NF-kappaB and neuropeptides appear to play a minor role in these mechanisms. PAR-2-mediated up-regulation of E-selectin and cell adhesion molecule ICAM-1; enhanced plasma extravasation was observed in humans and mice and of interleukin-6 in mice in vivo. Thus, PAR-2 may be a beneficial therapeutic target for the treatment of inflammatory skin diseases.
蛋白酶激活受体-2属于G蛋白偶联受体的一个新亚家族。其在炎症过程中的精确作用及潜在机制仍不清楚。我们的研究证实,PAR-2在小鼠和人类体内的皮肤炎症中发挥直接的促炎作用。在实验性诱导的过敏性(ACD)和毒性(ICD)接触性皮炎(CD)模型中,我们发现与野生型(PAR-2+/+)小鼠相比,PAR-2基因敲除突变体(PAR-2-/-)小鼠的耳部肿胀反应、血浆外渗和白细胞黏附明显减弱,尤其是在早期阶段。使用一氧化氮合酶抑制剂可显著减弱PAR-2激活所产生的促炎作用,而核因子κB和神经肽在这些机制中似乎起次要作用。在体内,PAR-2介导的E-选择素和细胞黏附分子ICAM-1上调;在人类和小鼠中均观察到血浆外渗增强,在小鼠中还观察到白细胞介素-6增加。因此,PAR-2可能是治疗炎症性皮肤病的一个有益的治疗靶点。