Salao Kanin, Watakulsin Krongkarn, Mairiang Eimorn, Suttiprapa Sutas, Tangkawattana Sirikachorn, Edwards Steven W, Sripa Banchob
Department of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
WHO Collaborating Centre for Research and Control of Opisthorchiasis (Southeast Asian Liver Fluke Disease), Tropical Disease Research Center, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Parasite Immunol. 2019 Jan;41(1):e12603. doi: 10.1111/pim.12603. Epub 2018 Dec 3.
Liver fluke infection caused by Opisthorchis viverrini induces several hepatobiliary conditions including advanced periductal fibrosis (APF) and cholangiocarcinoma (CCA), but >25% of the infected population develops APF and 1% develop CCA. The innate immune response is the first line of defence, and macrophages are critical regulators of fibrosis. We hypothesized that macrophages from infected individuals have different capacities to either promote or suppress periductal fibrosis. We compared phagocytic activities of macrophages of healthy individuals and O viverrini-infected individuals ± APF, and found that macrophages from infected individuals with APF ingested significantly higher numbers of beads compared with healthy controls and O viverrini-infected individuals without APF. To further investigate proteolytic activity, we monitored real-time phagosomal proteolysis of beads conjugated to DQ-BODIPY-BSA using live cell imaging. We show that macrophages from O viverrini-infected individuals with APF also have elevated phagosomal proteolysis activity, which is consistent with their increased phagocytic activity. Additionally, stimulated ROS production by blood monocytes was higher in individuals with APF compared with healthy controls and infected individuals without APF. These results suggest that during O viverrini infection, macrophages with high phagocytic and proteolytic activities together with elevated ROS production are the phenotypes that can promote tissue damage, which results in periductal fibrosis.
由麝猫后睾吸虫引起的肝吸虫感染会引发多种肝胆疾病,包括晚期胆管周围纤维化(APF)和胆管癌(CCA),但超过25%的受感染人群会发展为APF,1%会发展为CCA。先天免疫反应是第一道防线,巨噬细胞是纤维化的关键调节因子。我们假设,受感染个体的巨噬细胞促进或抑制胆管周围纤维化的能力不同。我们比较了健康个体以及感染麝猫后睾吸虫且伴有或不伴有APF的个体的巨噬细胞吞噬活性,发现伴有APF的受感染个体的巨噬细胞摄取的珠子数量显著高于健康对照组以及感染麝猫后睾吸虫但无APF的个体。为了进一步研究蛋白水解活性,我们使用活细胞成像监测了与DQ-硼二吡咯-牛血清白蛋白偶联的珠子的实时吞噬体蛋白水解过程。我们发现,伴有APF的感染麝猫后睾吸虫个体的巨噬细胞也具有更高的吞噬体蛋白水解活性,这与其增强的吞噬活性相一致。此外,与健康对照组以及感染麝猫后睾吸虫但无APF的个体相比,伴有APF的个体血液单核细胞刺激产生的活性氧(ROS)更高。这些结果表明,在麝猫后睾吸虫感染期间,具有高吞噬和蛋白水解活性以及增强的ROS产生的巨噬细胞是能够促进组织损伤从而导致胆管周围纤维化的表型。