Okuda Kazuhide S, Misa June Pauline, Oehlers Stefan H, Hall Christopher J, Ellett Felix, Alasmari Sultan, Lieschke Graham J, Crosier Kathryn E, Crosier Philip S, Astin Jonathan W
Department of Molecular Medicine & Pathology, School of Medical Sciences, University of Auckland, Auckland 1142, New Zealand.
Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham 27710, USA.
Biol Open. 2015 Sep 14;4(10):1270-80. doi: 10.1242/bio.013540.
Inflammatory bowel disease (IBD) is a disabling chronic inflammatory disease of the gastrointestinal tract. IBD patients have increased intestinal lymphatic vessel density and recent studies have shown that this may contribute to the resolution of IBD. However, the molecular mechanisms involved in IBD-associated lymphangiogenesis are still unclear. In this study, we established a novel inflammatory lymphangiogenesis model in zebrafish larvae involving colitogenic challenge stimulated by exposure to 2,4,6-trinitrobenzenesulfonic acid (TNBS) or dextran sodium sulphate (DSS). Treatment with either TNBS or DSS resulted in vascular endothelial growth factor receptor (Vegfr)-dependent lymphangiogenesis in the zebrafish intestine. Reduction of intestinal inflammation by the administration of the IBD therapeutic, 5-aminosalicylic acid, reduced intestinal lymphatic expansion. Zebrafish macrophages express vascular growth factors vegfaa, vegfc and vegfd and chemical ablation of these cells inhibits intestinal lymphatic expansion, suggesting that the recruitment of macrophages to the intestine upon colitogenic challenge is required for intestinal inflammatory lymphangiogenesis. Importantly, this study highlights the potential of zebrafish as an inflammatory lymphangiogenesis model that can be used to investigate the role and mechanism of lymphangiogenesis in inflammatory diseases such as IBD.
炎症性肠病(IBD)是一种使人衰弱的胃肠道慢性炎症性疾病。IBD患者的肠道淋巴管密度增加,最近的研究表明,这可能有助于IBD的缓解。然而,IBD相关淋巴管生成所涉及的分子机制仍不清楚。在本研究中,我们在斑马鱼幼虫中建立了一种新型的炎症性淋巴管生成模型,该模型涉及通过暴露于2,4,6-三硝基苯磺酸(TNBS)或硫酸葡聚糖钠(DSS)刺激引发的结肠炎。用TNBS或DSS处理均可导致斑马鱼肠道中血管内皮生长因子受体(Vegfr)依赖性淋巴管生成。给予IBD治疗药物5-氨基水杨酸可减轻肠道炎症,减少肠道淋巴扩张。斑马鱼巨噬细胞表达血管生长因子vegfaa、vegfc和vegfd,对这些细胞进行化学消融可抑制肠道淋巴扩张,这表明在致结肠炎刺激后巨噬细胞向肠道募集是肠道炎症性淋巴管生成所必需的。重要的是,本研究突出了斑马鱼作为炎症性淋巴管生成模型的潜力,可用于研究淋巴管生成在IBD等炎症性疾病中的作用和机制。