IL-1β suppression of VE-cadherin transcription underlies sepsis-induced inflammatory lung injury
Unchecked inflammation is a hallmark of inflammatory tissue injury in diseases such as
acute respiratory distress syndrome (ARDS). Yet the mechanisms of inflammatory lung injury
remain largely unknown. Here we showed that bacterial endotoxin lipopolysaccharide (LPS)
and cecal ligation and puncture–induced (CLP-induced) polymicrobial sepsis decreased the
expression of transcription factor cAMP response element binding (CREB) in lung
endothelial cells. We demonstrated that endothelial CREB was crucial for VE-cadherin …
acute respiratory distress syndrome (ARDS). Yet the mechanisms of inflammatory lung injury
remain largely unknown. Here we showed that bacterial endotoxin lipopolysaccharide (LPS)
and cecal ligation and puncture–induced (CLP-induced) polymicrobial sepsis decreased the
expression of transcription factor cAMP response element binding (CREB) in lung
endothelial cells. We demonstrated that endothelial CREB was crucial for VE-cadherin …
IL-1β suppression of VE-cadherin transcription underlies sepsis-induced inflammatory lung injury
Unchecked inflammation is a hallmark of inflammatory tissue injury in diseases such as
acute respiratory distress syndrome (ARDS). Yet the mechanisms of inflammatory lung injury
remain largely unknown. Here we showed that bacterial endotoxin lipopolysaccharide (LPS)
and cecal ligation and puncture–induced (CLP-induced) polymicrobial sepsis decreased the
expression of transcription factor cAMP response element binding (CREB) in lung
endothelial cells. We demonstrated that endothelial CREB was crucial for VE-cadherin …
acute respiratory distress syndrome (ARDS). Yet the mechanisms of inflammatory lung injury
remain largely unknown. Here we showed that bacterial endotoxin lipopolysaccharide (LPS)
and cecal ligation and puncture–induced (CLP-induced) polymicrobial sepsis decreased the
expression of transcription factor cAMP response element binding (CREB) in lung
endothelial cells. We demonstrated that endothelial CREB was crucial for VE-cadherin …