当前位置： SCI文献检索 > IMMUNOLOGY LETTERS期刊下所有文献 > Carbon monoxide ameliorates Staphylococcus aureus-elicited COX-2/IL-6/MMP-9-dependent human aortic endothelial cell migration and inflammatory responses.

Carbon monoxide ameliorates Staphylococcus aureus-elicited COX-2/IL-6/MMP-9-dependent human aortic endothelial cell migration and inflammatory responses.

Abstract：

:Staphylococcus aureus (S. aureus) can often lead to many life-threatening diseases. It has the ability to invade normal endovascular tissue. Acute inflammation and its resolution are important to ensure bacterial clearance and limit tissue injury. Carbon monoxide (CO) has been shown to exert anti-inflammatory effects in various tissues and organ systems. In our study, we investigated the effects and the mechanisms of carbon monoxide releasing molecule-2 (CORM-2) on S. aureus-induced inflammatory responses in human aortic endothelial cells (HAECs). We proved that S. aureus induced cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2)/interleukin-6 (IL-6)/matrix metallopeptidase-9 (MMP-9) expression and cell migration, which were decreased by CORM-2. Moreover, CORM-2 had no effects on TLR2 mRNA levels in response to S. aureus. Interestingly, we proved that S. aureus decreased intracellular ROS generation, suggesting that the inhibition of ROS further promoted inflammatory responses. However, CORM-2 significantly inhibited S. aureus-induced inflammation by increasing intracellular ROS generation. S. aureus-induced NF-κB activation was also inhibited by CORM-2. Finally, we proved that S. aureus induced levels of the biomarkers of inflammation in cardiovascular diseases, which were inhibited by CORM-2. Taken together, these results suggest that CORM-2 inhibits S. aureus-induced COX-2/PGE2/IL-6/MMP-9 expression and aorta inflammatory responses by increasing the ROS generation and reducing the inflammatory molecules levels.

journal_name

Immunol Lett

journal_title

Immunology letters

authors

Tsai MH,Yang CM,Chang KT,Chuang CC,Lin WN,Jiang RS,Wu CH,Lee IT

doi

10.1016/j.imlet.2018.09.010

subject

Has Abstract

pub_date

2018-11-01 00:00:00

pages

40-49

eissn

0165-2478

issn

1879-0542

pii

S0165-2478(18)30293-1

journal_volume

203

pub_type

杂志文章

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