Weinkopff Tiffany, Mackenzie Charles, Eversole Rob, Lammie Patrick J
Division of Parasitic Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia, United States of America; Department of Cell Biology, University of Georgia, Athens, Georgia, United States of America.
Department of Pathobiology and Diagnostic Investigation, Michigan State University, East Lansing, Michigan, United States of America; Department of Biological Sciences, Western Michigan University, Kalamazoo, Michigan, United States of America.
PLoS Negl Trop Dis. 2014 Jul 10;8(7):e2893. doi: 10.1371/journal.pntd.0002893. eCollection 2014 Jul.
The nematodes Wuchereria bancrofti and Brugia spp. infect over 120 million people worldwide, causing lymphedema, elephantiasis and hydrocele, collectively known as lymphatic filariasis. Most infected individuals appear to be asymptomatic, but many exhibit sub-clinical manifestations including the lymphangiectasia that likely contributes to the development of lymphedema and elephantiasis. As adult worm excretory-secretory products (ES) do not directly activate lymphatic endothelial cells (LEC), we investigated the role of monocyte/macrophage-derived soluble factors in the development of filarial lymphatic pathology. We analyzed the production of IL-8, IL-6 and VEGF-A by peripheral blood mononuclear cells (PBMC) from naïve donors following stimulation with filarial ES products. ES-stimulated PBMCs produced significantly more IL-8, IL-6 and VEGF-A compared to cells cultured in medium alone; CD14(+) monocytes appear to be the primary producers of IL-8 and VEGF-A, but not IL-6. Furthermore, IL-8, IL-6 and VEGF-A induced in vitro tubule formation in LEC Matrigel cultures. Matrigel plugs supplemented with IL-8, IL-6, VEGF-A, or with supernatants from ES-stimulated PBMCs and implanted in vivo stimulated lymphangiogenesis. Collectively, these data support the hypothesis that monocytes/macrophages exposed to filarial ES products may modulate lymphatic function through the secretion of soluble factors that stimulate the vessel growth associated with the pathogenesis of filarial disease.
班氏吴策线虫和布鲁格氏丝虫属线虫在全球感染了超过1.2亿人,导致淋巴水肿、象皮病和鞘膜积液,统称为淋巴丝虫病。大多数感染者似乎没有症状,但许多人表现出亚临床症状,包括淋巴管扩张,这可能导致淋巴水肿和象皮病的发展。由于成虫的排泄分泌产物(ES)不会直接激活淋巴管内皮细胞(LEC),我们研究了单核细胞/巨噬细胞衍生的可溶性因子在丝虫性淋巴病理发展中的作用。我们分析了来自未接触过丝虫的供体的外周血单个核细胞(PBMC)在用丝虫ES产物刺激后IL-8、IL-6和VEGF-A的产生情况。与仅在培养基中培养的细胞相比,ES刺激的PBMC产生的IL-8、IL-6和VEGF-A显著更多;CD14(+)单核细胞似乎是IL-8和VEGF-A的主要产生者,但不是IL-6的主要产生者。此外,IL-8、IL-6和VEGF-A在LEC基质胶培养物中诱导体外小管形成。补充有IL-8、IL-6、VEGF-A或ES刺激的PBMC上清液的基质胶栓植入体内后刺激了淋巴管生成。总体而言,这些数据支持以下假设:暴露于丝虫ES产物的单核细胞/巨噬细胞可能通过分泌可溶性因子来调节淋巴功能,这些可溶性因子刺激与丝虫病发病机制相关的血管生长。