Collado-Cuadrado Manuel, Alarcón-Torrecillas Claudia, Rodríguez-Escolar Iván, Balmori-de la Puente Alfonso, Infante González-Mohino Elena, Pericacho Miguel, Morchón Rodrigo
Zoonotic Diseases and One Health Group, Faculty of Pharmacy, University of Salamanca, 37007 Salamanca, Spain.
Centre for Environmental Studies and Rural Dynamization (CEADIR), University of Salamanca, 37007 Salamanca, Spain.
Pathogens. 2024 Jul 22;13(7):603. doi: 10.3390/pathogens13070603.
Heartworm disease caused by is a vector-borne zoonotic disease responsible for the infection of mainly domestic dogs and cats, or these are those for which the most data are known. Humans are an accidental host where a benign, asymptomatic pulmonary nodule may originate. also harbours the endosymbiont bacteria of the genus , which play a role in moulting, embryogenesis, inflammatory pathology, and immune response. When sp. is released into the bloodstream, endothelial and pulmonary damage is exacerbated, further encouraging thrombus formation and pulmonary hypertension, facilitating congestive heart failure and death of the animal. Previous studies have shown that parasite excretory/secretory products are able to activate the pro-angiogenic pathway (formation of new vessels) to facilitate parasite survival. The aim of this study was to analyse the role of sp. and its relationship with the cellular processes and the angiogenic pathway in a model of human endothelial cells in vitro. The use of recombinant Surface Protein (rWSP) showed that its stimulation exerted an anti-angiogenic effect by detecting an increase in the production of VEGFR-1/sFlt1 and sEndoglin and did not affect the production of VEGFR-2 and mEndoglin (pro-angiogenic molecules). Furthermore, it did not stimulate cell proliferation or migration, although it did negatively stimulate the formation of pseudocapillaries, slowing down this process. These cellular processes are directly related to the angiogenic pathway so, with these results, we can conclude that sp. is related to the stimulation of the anti-angiogenic pathway, not facilitating the survival of in vascular endothelium.
由[寄生虫名称未给出]引起的心丝虫病是一种媒介传播的人畜共患病，主要感染家犬和家猫，或者说这些动物是已知数据最多的宿主。人类是偶然宿主，可能会出现良性、无症状的肺结节。[寄生虫名称未给出]还携带[细菌属名称未给出]的内共生细菌，这些细菌在蜕皮、胚胎发育、炎症病理学和免疫反应中发挥作用。当[寄生虫名称未给出]物种释放到血液中时，会加剧内皮和肺部损伤，进一步促进血栓形成和肺动脉高压，导致动物充血性心力衰竭和死亡。先前的研究表明，寄生虫排泄/分泌产物能够激活促血管生成途径（新血管形成）以促进寄生虫存活。本研究的目的是在体外人内皮细胞模型中分析[寄生虫名称未给出]物种的作用及其与细胞过程和血管生成途径的关系。使用重组[寄生虫名称未给出]表面蛋白（rWSP）表明，通过检测VEGFR-1/sFlt1和sEndoglin的产生增加，其刺激发挥了抗血管生成作用，并且不影响VEGFR-2和mEndoglin（促血管生成分子）的产生。此外，它不刺激细胞增殖或迁移，尽管它确实对伪毛细血管的形成产生负面刺激，减缓了这一过程。这些细胞过程与血管生成途径直接相关，因此，根据这些结果，我们可以得出结论，[寄生虫名称未给出]物种与抗血管生成途径的刺激有关，不利于[寄生虫名称未给出]在血管内皮中的存活。
