Abstract:
:Acute lung injury (ALI) remains a serious health issue with little improvement in our understanding of the pathophysiology and therapeutic approaches. We investigated the mechanism that lipopolysaccharide (LPS) induces early neutrophil recruitment to lungs and increases pulmonary vascular permeability during ALI. Intratracheal LPS induced release of pro-interleukin-1α (IL-1α) from necrotic alveolar macrophages (AM), which activated endothelial cells (EC) to induce vascular leakage via loss of vascular endothelial (VE)-cadherin. LPS triggered the AM purinergic receptor P2X7(R) to induce Ca(2+) influx and ATP depletion, which led to necrosis. P2X7R deficiency significantly reduced necrotic death of AM and release of pro-IL-1α into the lung. CD14 was required for LPS binding to P2X7R, as CD14 neutralization significantly diminished LPS induced necrotic death of AM and pro-IL-1α release. These results demonstrate a key role for pro-IL-1α from necrotic alveolar macrophages in LPS-mediated ALI, as a critical initiator of increased vascular permeability and early neutrophil infiltration.
journal_name
Immunityjournal_title
Immunityauthors
Dagvadorj J,Shimada K,Chen S,Jones HD,Tumurkhuu G,Zhang W,Wawrowsky KA,Crother TR,Arditi Mdoi
10.1016/j.immuni.2015.03.007subject
Has Abstractpub_date
2015-04-21 00:00:00pages
640-53issue
4eissn
1074-7613issn
1097-4180pii
S1074-7613(15)00121-1journal_volume
42pub_type
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