Program in Translational Lung Research, Department of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
Front Immunol. 2019 Jan 24;10:27. doi: 10.3389/fimmu.2019.00027. eCollection 2019.
Approximately 5% of individuals chronically infected with develop pulmonary hypertension (PH). The disease is progressive and often fatal, and treatment options are palliative, not curative. Recent studies have unraveled major players of the Th2 inflammation axis in the -induced PH pathology using murine models and studying human samples. TGF-β signaling is a link between the Type 2 inflammation and vascular remodeling, and specifically Thrombospondin-1 (TSP-1) is upregulated by the inflammation and activates TGF-β. Overall, the current model for the pathogenesis of -induced PH is that deposition of eggs in the pulmonary vasculature results in localized Th2 inflammation, leading to TGF-β activation by TSP-1, and the active TGF-β then results in vascular remodeling and PH.
约 5%的慢性感染 个体发展为肺动脉高压（PH）。该病呈进行性发展，且常致命，治疗方法仅为姑息，而非治愈。最近的研究使用鼠模型和研究人类样本，揭示了 Th2 炎症轴在 诱导的 PH 病理中的主要参与者。TGF-β信号转导是 2 型炎症和血管重塑之间的联系，特别是血小板反应蛋白-1（TSP-1）被炎症上调并激活 TGF-β。总的来说，目前 诱导的 PH 发病机制模型是， 在肺血管中沉积的 卵导致局部 Th2 炎症，导致 TSP-1 激活 TGF-β，而活性 TGF-β 则导致血管重塑和 PH。
