Eosinophils Restrict Diesel Exhaust Particles-induced Cell Proliferation of Lung Epithelial A549 Cells via Interleukin-13 Mediated Mechanisms: Implications for Tissue Remodeling and Fibrosis

Abstract

Background:Diesel exhaust particles (DEPs) affect lung physiology and cause serious damage to the lungs. A number of studies demonstrated that eosinophils play a very important role in the development of tissue remodeling and fibrosis of the lungs. However, the exact mechanism of pathogenesis of tissue remodeling and fibrosis is not known.Methods:Both in vitro and in vivo models were used in the study. HL-60 and A549 cells were also utilized in the study. 8 to 12 weeks old BALB/c mice were used for the in vivo study. Cell viability by MTT assay and RNA isolation by tri reagent was accomplished. mRNA expression of inflammatory genes was accomplished by real-time PCR or qPCR. Immunohistochemistry was done to assess the localization and expressions of proteins. One-way ANOVA followed by a post hoc test was done for the statistical analysis. Graph-Pad prism 5 software was used for statistical analysis.Results:Altogether, we elucidated the mechanistic role of eosinophils and IL-13 in the DEP-triggered proliferation of lungs cells, thus providing an insight into the pathophysiology of tissue remodeling and fibrosis of lungs.Conclusion:Altogether, we elucidated, the mechanistic role of eosinophils and IL-13 in the DEP-triggered proliferation of lungs cells thus providing an inside in the pathophysiology of tissue remodelling and fibrosis of lungs.