吞噬作用
STAT蛋白
信号转导
免疫印迹
生物
分子生物学
CD64
车站3
微生物学
细胞生物学
流式细胞术
生物化学
基因
作者
Qingsong Lei,Lin Li,Wenxiang Huang,Bo Qin,Shujun Zhang
摘要
Abstract Hepatitis E virus (HEV) could induce chronic hepatitis and liver failure with high mortality through unknown mechanisms. The previous study showed that the HEV open reading frames 3 (ORF3) could inhibit macrophages inflammatory response. Impaired macrophages phagocytosis was also found in patients infected with HEV and its nucleic acids could be detected in macrophages. To elucidate the role of HEV ORF3 on phagocytosis, the phagocytosis activation was measured by phagocytosis test, flow cytometry, and phalloidin staining. Meanwhile, the expression of key phagocytic receptors and the activation of transduction pathway were investigated by using reverse transcription real‐time quantitative polymerase chain reaction (RT‐qPCR) and Western blot analysis. Results of phagocytosis test showed that the HEV ORF3 could significantly impair the absorption capacity of latex beads. Furthermore, results of RT‐qPCR and Western blot analysis showed that the expression of CD14 and CD64 decreased. Afterward, the present study showed that the activation of Janus kinase‐signal transducer and activator of transcription (JAK/STAT) signaling pathway was inhibited by HEV ORF3 and downregulation of CD14 and CD64 could be reversed by interferon γ, one activator of the JAK1/STAT1 signaling pathway. In conclusion, HEV ORF3 could significantly impair the phagocytosis of macrophage by downregulating expression of CD14 and CD64, which may function by inhibiting the activation of the JAK1/STAT1 signaling pathway.
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