炎症
纤维化
曼氏血吸虫
肝纤维化
肝纤维化
病理
医学
血吸虫病
肝硬化
免疫学
肝星状细胞
化学
生物
蠕虫
作者
Diego S. Ferreira,Gunisha Arora,Richard L. Gieseck,Nicholas J. Rotile,Philip A. Waghorn,Kenneth K. Tanabe,Thomas A. Wynn,Peter Caravan,Bryan C. Fuchs
标识
DOI:10.1097/rli.0000000000000737
摘要
Three groups of mice that develop either mild type 2 inflammation and fibrosis (wild type), severe fibrosis with exacerbated type 2 inflammation (Il10-/-Il12b-/-Il13ra2-/-), or minimal fibrosis with marked type 1 inflammation (Il4ra∂/∂) after infection with S. mansoni were imaged using both probes for determination of signal enhancement. Schistosoma mansoni-infected wild-type mice developed chronic liver fibrosis.The liver MR signal enhancement after either probe administration was significantly higher in S. mansoni-infected wild-type mice compared with naive animals. The S. mansoni-infected Il4ra∂/∂ mice presented with little liver signal enhancement after probe injection despite the presence of substantial inflammation. Schistosoma mansoni-infected Il10-/-Il12b-/-Il13ra2-/- mice presented with marked fibrosis, which correlated to increased signal enhancement after injection of either probe.Both MR probes, EP-3533 and Gd-Hyd, were specific for fibrosis in this model of chronic liver disease regardless of the presence or severity of the underlying inflammation. These results, in addition to previous findings, show the potential application of both molecular MR probes for detection and quantification of fibrosis from various etiologies.
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