Infection with Staphylococcus aureus elicits COX-2/PGE2/IL-6/MMP-9-dependent aorta inflammation via the inhibition of intracellular ROS production - 20/09/18
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Graphical abstract |
Highlights |
• | S. aureus induces aorta inflammation by decreasing ROS generation. |
• | S. aureus promotes MMP-9 expression via the induction of PGE2/IL-6. |
• | S. aureus promoted aorta inflammation via p38 MAPK, ERK1/2, and NF-κB activation. |
• | COX-2/PGE2 can promote IL-6/MMP-9-dependent cell migration. |
Abstract |
Staphylococcus aureus (S. aureus) can lead to many life-threatening diseases. It has the ability to invade normal endovascular tissue. The molecular mechanisms and pathological changes of endothelial cells after S. aureus infection are of interest, but the basic understanding of how S. aureus destroys this barrier is not clear. Here, we showed that S. aureus enhanced COX-2 expression and prostaglandin E2 (PGE2) secretion in human aortic endothelial cells (HAECs). In addition, S. aureus induced PGE2/interleukin-6 (IL-6)/matrix metallopeptidase-9 (MMP-9)-dependent cell migration. S. aureus-induced COX-2, IL-6, and MMP-9 levels were inhibited by transfection with siRNA of Toll-like receptor 2 (TLR2), p38, p42, p44, p50, or p65. S. aureus also induced p38 MAPK, ATF2, ERK1/2, and NF-κB p65 activation. Interestingly, we proved that S. aureus decreased intracellular generation of reactive oxygen species (ROS), which suggests that the inhibition of ROS production promoted inflammatory responses. Finally, we showed that S. aureus enhanced a variety of biomarkers of inflammation in cardiovascular diseases. However, the free radical scavenger (MCI-186) or antioxidant (N-acetyl-L-cysteine, NAC) markedly enhanced S. aureus-induced COX-2 mRNA levels in the aorta tissues. Taken together, these findings established that S. aureus promoted aorta inflammation via activation of p38 MAPK, ERK1/2, and NF-κB and inhibition of ROS generation.
Le texte complet de cet article est disponible en PDF.Keywords : Staphylococcus aureus, Cyclooxygenase-2, Matrix metallopeptidase-9, Aorta inflammation, Interleukin-6
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Vol 107
P. 889-900 - novembre 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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