Fernandes Jamille Souza, Araujo Maria Ilma, Lopes Diego Mota, de Souza Robson da Paixão, Carvalho Edgar M, Cardoso Luciana Santos
Serviço de Imunologia, Complexo Hospitalar Universitário Professor Edgard Santos, Universidade Federal da Bahia, Rua João das Botas s/n, Canela, 40110-160 Salvador, BA, Brazil.
Serviço de Imunologia, Complexo Hospitalar Universitário Professor Edgard Santos, Universidade Federal da Bahia, Rua João das Botas s/n, Canela, 40110-160 Salvador, BA, Brazil ; Instituto Nacional de Ciência e Tecnologia em Doenças Tropicais (INCT-DT), CNPQ/MCT, Brazil ; Escola Bahiana de Medicina e Saúde Pública, 40050-420 Salvador, BA, Brazil.
Mediators Inflamm. 2014;2014:703653. doi: 10.1155/2014/703653. Epub 2014 Mar 13.
A major issue with Schistosoma mansoni infection is the development of periportal fibrosis, which is predominantly caused by the host immune response to egg antigens. Experimental studies have pointed to the participation of monocytes in the pathogenesis of liver fibrosis. The aim of this study was to characterize the subsets of monocytes in individuals with different degrees of periportal fibrosis secondary to schistosomiasis. Monocytes were classified into classical (CD14(++)CD16(-)), intermediate (CD14(++)CD16(+)), and nonclassical (CD14(+)CD16(++)). The expressions of monocyte markers and cytokines were assessed using flow cytometry. The frequency of classical monocytes was higher than the other subsets. The expression of HLA-DR, IL-6, TNF-α, and TGF-β was higher in monocytes from individuals with moderate to severe fibrosis as compared to other groups. Although no differences were observed in receptors expression (IL-4R and IL-10R) between groups of patients, the expression of IL-12 was lower in monocytes from individuals with moderate to severe fibrosis, suggesting a protective role of this cytokine in the development of fibrosis. Our data support the hypothesis that the three different monocyte populations participate in the immunopathogenesis of periportal fibrosis, since they express high levels of proinflammatory and profibrotic cytokines and low levels of regulatory markers.
曼氏血吸虫感染的一个主要问题是门周纤维化的发展,这主要是由宿主对虫卵抗原的免疫反应引起的。实验研究表明单核细胞参与了肝纤维化的发病机制。本研究的目的是对血吸虫病继发不同程度门周纤维化个体的单核细胞亚群进行特征分析。单核细胞被分为经典型(CD14(++)CD16(-))、中间型(CD14(++)CD16(+))和非经典型(CD14(+)CD16(++))。使用流式细胞术评估单核细胞标志物和细胞因子的表达。经典单核细胞的频率高于其他亚群。与其他组相比,中度至重度纤维化个体的单核细胞中HLA-DR、IL-6、TNF-α和TGF-β的表达更高。尽管在患者组之间未观察到受体表达(IL-4R和IL-10R)的差异,但中度至重度纤维化个体的单核细胞中IL-12的表达较低,提示该细胞因子在纤维化发展中具有保护作用。我们的数据支持这一假设,即三种不同的单核细胞群体参与了门周纤维化的免疫发病机制,因为它们表达高水平的促炎和促纤维化细胞因子以及低水平的调节标志物。