Porcine reproductive and respiratory syndrome virus (PRRSV) up-regulates IL-8 expression through TAK-1/JNK/AP-1 pathways.
The acute phase of respiratory distress caused by porcine reproductive and respiratory syndrome virus (PRRSV) is likely a consequence of the release of inflammatory cytokines in the lung. IL-8, the main chemokine and activator of neutrophils, might be related to the lung injury upon PRRSV infection. In this study, we showed that PRRSV induced IL-8 expression in vivo and in vitro. Subsequently, we demonstrated that JNK and NF-κB pathways were activated upon PRRSV infection and required for the enhancement of IL-8 expression. We further verified that PRRSV-activated TAK-1 was essential for the activation of JNK and NF-κB pathways and IL-8 expression. Moreover, we revealed an AP-1 binding motif in the cloned porcine IL-8 (pIL-8) promoter, and deletion of this motif abolished the pIL-8 promoter activity. Finally, we found that the JNK-activated AP-1 subunit c-Jun was critical for the up-regulation of IL-8 expression by PRRSV. These data suggest that PRRSV-induced IL-8 production is likely through the TAK-1/JNK/AP-1 pathways.
['Liu|Yihao|Y|', 'Du|Yinping|Y|', 'Wang|Honglei|H|', 'Du|Li|L|', 'Feng|Wen-Hai|WH|']
D000818:Animals D016209:Interleukin-8 D048031:JNK Mitogen-Activated Protein Kinases D020930:MAP Kinase Kinase Kinases D019318:Porcine Reproductive and Respiratory Syndrome D019316:Porcine respiratory and reproductive syndrome virus D015398:Signal Transduction D013552:Swine D018808:Transcription Factor AP-1 D015854:Up-Regulation
PRRSV IL-8 TAK-1 JNK AP-1