Effects of Adenovirus-Mediated Overexpression of JAZF1 on Chronic Inflammation: An In Vitro and In Vivo Study

BACKGROUND: Insulin sensitivity and inflammation can be affected by juxtaposition with another zinc finger gene 1 (JAZF1), but its precise role in chronic inflammation is unclear. In this study, JAZF1-overexpression adenovirus plasmids were transfected into macrophages, CD4(+) T cells, and C57BL/6J mice to assess the role of JAZF1 in chronic inflammation. MATERIAL/METHODS: JAZF1 was cloned into an adenovirus skeleton plasmid and transfected in HEK293 cells to package and enrich the virus particles. In vitro, the JAZF1 overexpression adenovirus vector (PAD-JAZF1) was cultured with peritoneal macrophages and peripheral blood CD4(+) T cells of C57BL/6J mice, and samples were evaluated using flow cytometry. In vivo, PAD-JAZF1 was introduced into C57BL/6J mice, and livers were collected to evaluate factors related to inflammation by hematoxylin & eosin and immunohistochemical staining. RESULTS: In vitro, PAD-JAZF1 decreased total macrophages, CD11c(+) macrophages, and the secretion of proinflammatory cytokines, but increased CD206(+) macrophages. It also decreased total CD4(+) T cells, active T cells, memory T cells, and the secretion of IL-6, IL-10, and IFN-γ, but increased Treg cells and restrictive T cells. In vivo, compared to those in the control group transfected with the adenovirus skeleton vector, mice transfected with the PAD-JAZF1 recombinant adenovirus had fewer CD11c(+) ATMs and CD4(+) T cells, lower levels of TNF-α and IL-6, and higher IL-10 concentrations in the liver. CONCLUSIONS: These findings indicate that JAZF1 limits chronic inflammation by reducing macrophage and CD4(+) T cell populations, altering subtype differentiation, and regulating the secretion of immune-related factors.