PT  - JOURNAL ARTICLE
AU  - Xiaolin He
AU  - Shi Wang
AU  - Shuyue Xia
AU  - Xu Liu
AU  - Ning Song
TI  - PTX3 as a component of innate immunity in the role of captopril in acute lung injury induced by bacterial endotoxin
DP  - 2011 Sep 01
TA  - European Respiratory Journal
PG  - p819
VI  - 38
IP  - Suppl 55
4099  - http://erj.ersjournals.com/content/38/Suppl_55/p819.short
4100  - http://erj.ersjournals.com/content/38/Suppl_55/p819.full
SO  - Eur Respir J2011 Sep 01; 38
AB  - Objective: Innate immunity is an important mechanism for the development of acute lung injury (ALI). Long pentraxin PTX3 is an inflammatory mediator and a component of innate immunity. Recent evidence implies that angiotensin-converting enzyme (ACE) plays an important role in the pathogenesis of ALI. We speculated that inhibition of ACE play the protective effect on ALI through the presence of PTX3, therefore, protect the lung from severe injury.Methods: Lung injury was induced by intratracheal instillation of lipopolysaccharide (LPS) in rats, followed by i.p. administration of captopril, an ACE inhibitor, or saline control, and the PTX3 expression, fibrin deposition, tissue factor expression and lung injury were determined. Local and systemic inflammatory responses were assessed by measuring cytokines in the lung and plasma.Results: Treatment with captopril dramatically attenuated LPS-induced lung injury, alveolar fibrin deposition and inflammatory cell infiltration 6 h after LPS challenge compared to that in the saline control rats. Local and systemic PTX3 expression were significantly decreased by the captopril therapy, accompanied by decreased interleukin (IL)-6, IL-10 and monocyte chemoattractant protein-1 levels in the plasma.Conclusion: These results support that inhibition of ACE with its clinically used inhibitor offers protective effects on ALI; PTX3, acting as both anti-inflammation component and the component of innate immunity, may reflect severity of lung injury and serve as the potential therapeutic “target” during ALI. Captopril treatment through the presence of PTX3 could be a potential mechanism that mediates lung injury.