[Progress in researches on macrophages in liver fibrosis of schistosomiasis].

Schistosomiasis causes the imbalance of fibrogenesis and pro-fibrinolytic promoting factors, leading to extracellular matrix deposition and liver fibrosis. The activation of liver macrophages (Kupffer cells) and stellate cells are the two crucial events, which constitute a complex network regulating fibrosis balance. This review discusses the function of fibrotic cytokines secreted by macrophages, and their interaction and mutual influence with stellate cells in hepatic fibrosis.

Comparative studies of macrophage-biased responses in mice to infection with Toxoplasma gondii ToxoDB #9 strains of different virulence isolated from China.

Background: Different from three clonal lineages of Toxoplasma gondii in North America and Europe, the genotype China 1 is predominantly prevalent in China. However, there are different virulent isolates within China 1, such as virulent TgCtwh3 and avirulent TgCtwh6, and little is known about differences in macrophage activation between them. The objective of this study focused on cytokine production, phenotype and markers of activated macrophages, and correlated signaling pathway induced by the two isolates.

Tim-2 up-regulation and galectin-9-Tim-3 pathway activation in Th2-biased response in Schistosoma japonicum infection in mice.

T cell immunoglobulin domain and mucin domain (Tim) family, a new gene that expresses on the surface of T cells, plays a critical role in regulation of T cells response. Previous data have shown that Tim-3 expressed on Th1 cells promotes itself apoptosis. Tim-2 is preferentially up-regulated during Th2 differentiation and functions as a potent costimulatory molecule for T-cell immunity.

Evaluation of recombinant SjLAP and SjFBPA in detecting antibodies to Schistosoma japonicum.

Objective: To investigate the early response of immunoglobulin G (IgG) antibody responses to Schistosoma japonicum infection in mice by using the recombinant proteins, S. japonicum leucine aminopeptidase (rSjLAP) and S. japonicum fructose-1, 6-bisphosphate aldolase (rSjFBPA), and evaluate the potential of rSjLAP and rSjFBPA in diagnosis as well as in assessment of therapeutic efficacy in human schistosomiasis.

[Inhibitory effect of paeoniflorin on the collagen production by fibroblasts through IL-13/STAT6 signaling pathway].

Objective: To observe the effects of paeoniflorin on 3T3 fibroblast activation, proliferation and collagen production through IL-13/STAT6 signaling pathway.

Methods: 3T3 cell strain was cultured with serum-free medium for 12 h, then stimulated by paeoniflorin (200, 400, 600, 800, and 1000 mg/L) or rIL-13 (6.25, 12.

[Effect of paeoniflorin on hepatic immunopathogenesis in mice with Schistosoma japonicum infection].

Objective: To investigate the mechanism of paeoniflorin in preventing hepatic granuloma formation and fibrosis in mice infected with Schistosoma japonicum.

Methods: Model of hepatic granuloma and fibrosis was established by infecting mice with S. japonicum cercariae.

[Effect of paeoniflorin on secretion of TGF-beta1 from macrophages in mice].

Objective: To explore the effect of paeoniflorin (PAE) on the production of transforming growth factor beta1 (TGF-beta1) from peritoneal macrophages(PMs) stimulated by soluble egg antigen (SEA) of Schistosoma japonicum.

Methods: SEA was prepared by trituration and added into culture plank, flask and dish containing PMs which were cultured for 24 h. TGF-beta1 secreted from PMs was measured by ELISA.

[Secreted expression of signaling protein 14-3-3 of Schistosoma japonicum in Pichia pastoris system with primary evaluation on its antigenicity].

Objective: To express signaling protein Sj14-3-3 in Pichia pastoris and compare its antigenicity with prokaryotic expression one.

Methods: Sj14-3-3 gene was amplified from pET28a-Sj14-3-3 recombinant plasmid, cloned into vector pMD18-T followed by sequencing. The Sj14-3-3 gene was subcloned into the expression vector pPICZalpha-B and transformed into Pichia pastoris X-33 by electroporation.