scholarly journals Secretory Phospholipase A2 Enzymes in Acute Lung Injury

Author(s):  
Eleftheria Letsiou ◽  
Yu Maw Htwe ◽  
Steven M. Dudek
2003 ◽  
Vol 21 (6) ◽  
pp. 1040-1045 ◽  
Author(s):  
H.L. Attalah ◽  
Y. Wu ◽  
M. Alaoui-El-Azher ◽  
F. Thouron ◽  
K. Koumanov ◽  
...  

2012 ◽  
Vol 52 (5) ◽  
pp. 729-737 ◽  
Author(s):  
Daniele De Luca ◽  
Angelo Minucci ◽  
Joaquim Trias ◽  
Domenico Tripodi ◽  
Giorgio Conti ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1731
Author(s):  
Yu Maw Htwe ◽  
Huashan Wang ◽  
Patrick Belvitch ◽  
Lucille Meliton ◽  
Mounica Bandela ◽  
...  

Lung endothelial dysfunction is a key feature of acute lung injury (ALI) and clinical acute respiratory distress syndrome (ARDS). Previous studies have identified the lipid-generating enzyme, group V phospholipase A2 (gVPLA2), as a mediator of lung endothelial barrier disruption and inflammation. The current study aimed to determine the role of gVPLA2 in mediating lung endothelial responses to methicillin-resistant Staphylococcus aureus (MRSA, USA300 strain), a major cause of ALI/ARDS. In vitro studies assessed the effects of gVPLA2 inhibition on lung endothelial cell (EC) permeability after exposure to heat-killed (HK) MRSA. In vivo studies assessed the effects of intratracheal live or HK-MRSA on multiple indices of ALI in wild-type (WT) and gVPLA2-deficient (KO) mice. In vitro, HK-MRSA increased gVPLA2 expression and permeability in human lung EC. Inhibition of gVPLA2 with either the PLA2 inhibitor, LY311727, or with a specific monoclonal antibody, attenuated the barrier disruption caused by HK-MRSA. LY311727 also reduced HK-MRSA-induced permeability in mouse lung EC isolated from WT but not gVPLA2-KO mice. In vivo, live MRSA caused significantly less ALI in gVPLA2 KO mice compared to WT, findings confirmed by intravital microscopy assessment in HK-MRSA-treated mice. After targeted delivery of gVPLA2 plasmid to lung endothelium using ACE antibody-conjugated liposomes, MRSA-induced ALI was significantly increased in gVPLA2-KO mice, indicating that lung endothelial expression of gVPLA2 is critical in vivo. In summary, these results demonstrate an important role for gVPLA2 in mediating MRSA-induced lung EC permeability and ALI. Thus, gVPLA2 may represent a novel therapeutic target in ALI/ARDS caused by bacterial infection.


2000 ◽  
Vol 41 (11) ◽  
pp. 1849-1857 ◽  
Author(s):  
Frederick C. de Beer ◽  
Patrice M. Connell ◽  
J. Yu ◽  
Maria C. de Beer ◽  
Nancy R. Webb ◽  
...  

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