Expression Of CXCL10/CXCR3 In PRRSV Infected Porcine Lung Tissues And The Macrophages

CXCL10 is one of chemokines, its main functions are medicated by its only receptor, chemokine receptor 3(CXCR3).CXCL10 plays important role in several cellular functions including cell migration, growth, differentiation, and death. In addition, it also regulates such as virus infection, inflammation, tumor, wound repair, and autoimmune disease.CXCL10/CXCR3 signaling in a variety of infection by viruses plays an important role in lung injury, and pig lung injury caused by PRRSV infection is a major cause of death in the infected pigs, the roles of CXCL10/CXCR3 in the process of lung injure has yet to be clear. This study to examine the expression of CXCL10 and CXCR3 at the level of mRNA and protein in PRRSV artificial infected and naturally infected pig lung tissues. In addition, their expression is also examined in inflammatory macrophages.1. The expression of CXCL10 and CXCR3 in the pig lung tissue with infection of PRRSVUsing qPCR method and Western blot we examine the expressions of CXCL10 and CXCR3 in the lung tissue with artificial PRRSV infection or clinical infection. We found that CXCL10 is higher expression in both artificial and clinical infection group, and CXCR3 is only higher expression in artificial infection but not in clinical infection. These results suggest that there are different regulation of CXCL10 and CXCR3 expression in lung injure caused by PRRSV infection.2. Regulation of the expression of CXCL10 and CXCR3 in macrophages stimulated by Poly(I:C) or LPS.The expression levels of CXCL10 and CXCR3 were significantly increased in macrophages stimulated by Poly(I:C). In contrast, the expression levels of CXCL10 and CXCR3 were significantly decreased in macrophages stimulated by LPS. The results showed that Poly(I:C) can promote the expression of CXCL10 and CXCR3, LPS can inhibit their expression.3. LPS inhibites the expression of CXCL10 and CXCR3 induced by Poly(I:C)This study uses the qPCR assey was applied to detection the mRNA expression of CXCL10 and CXCR3 by the Poly(I:C) and LPS costimulation of macrophages. Compare to Poly(I:C) alone stimulated cells, CXCL10 and CXCR3 mRNA expressions are significantly reduced. The results suggest that LPS could inhibit the Poly(I:C)-induced expression of CXCL10 and CXCR3.4. Effects of diffirent treatment of Poly(I:C), LPS, or both on the viability of macrophages.In order to study the toxic effects of Poly(I:C), LPS and Poly(I:C)-LPS costimulation on the cell viability of macrophages, we use MTT assay to evaluate cell viability. Poly(I:C) stimulating cell shows no obvious change after the cell vitality, LPS and Poly(I:C)-LPS costimulating cells show that the cell vitality is reduced to 60%. The effects of LPS on cell viability may affect the expression of CXCL10 and CXCR3 in macrophages.In summary, the expression of CXCL10 and CXCR3 in macrophage by Poly(I:C) can simulate the artificial infection of PRRSV in lung tissue. We can use this cell model to study the regulation of expression of CXCL10 and CXCR3 in artificial infected PRRSV. The model of clinical outcomes remains to be further studied, and the effect of the change of CXCL10/CXCR3 axis expression is not yet clear, but also needs to be further studied.