Expression Of Interleukin-32 Induced By TNF-A Via Akt And Jnk Activation In Human Lung Fibroblasts

Subject:Respiratory disease is a global disease, millions of people in the world suffered by it. COPD is a leading cause of morbidity and mortality worldwide and is expected to become the third leading cause of death in 2020. Around 300 million people currently have asthma, leading 180000 deaths worldwide each year. Human lung fibroblasts is not only the structure of lung cells, but also the important participants of lung innate immunity.IL-32 as a crucial pro-inflammatory factor in airway inflammation, its role in human lung fibroblasts has not yet been reported. TNF-a is the key regulator in the progress of airway inflammation. The regulating mechanism of expression IL-32 by TNF-a in Human lung Fibroblasts in airway inflammation diseases.Methods:Q-PCR test the expression of IL-32mRNA induced by inflammation stimulating factor in Human lung fibroblasts;IL-32protein secreted in supernatant by ELISA; Western blot show the signal pathway phosphorylation protein in PVDF membrane.Results:To some extent, TNF-a induced Human lung fibroblasts express IL-32mRNA of 4 spliced isoforms (α、β、γ and δ) in dose dependence. Expression of IL-32 induced by TNF-ain Human lung fibroblasts, but IL-32adose not exist in supernatant. We didn’t found any other synergetic stimulating factors with TNF-a. Furthermore, the activation of Akt and JNK pathways regulated TNF-a-induced IL-32 expression in human lung fibroblasts, and inhibition of the Akt and JNK pathways was able to suppress the increased release of IL-32 to nearly the basal level.Conclusion:Expression of Interleukin-32 Induced by TNF-a via AKT and JNK Activation in Human Lung Fibroblasts...