WB 04. Chemokine Involvement in Lung Injury Secondary to Ischaemia/Reperfusion

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S. Paredes, L. Rancan, L. Huerta, D. Rincón, C. Garcia, I. Garutti, C. Simón, E. Vara

Chair(s): Mustafa Cikirikcioglu, Frank Dor, Attila Szijarto, David J. Hackam, Cliff Shearman, Modise Koto, Yuzo Yamamoto

9:56 - 10:10h at Erszebet Room (A)

Categories: Walter Brendel Award, Thoracic Surgery

Session: Walter Brendel Award

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Background
Ischaemia and reperfusion (I/R) elicit an acute inflammatory response characterized by the recruitment of inflammatory cells, oxidative stress and endothelial barrier failure that can lead to interstitial oedema and impairment of organ function. Neutrophils are known to mediate the organ injury, but the precise mechanisms leading to lung neutrophil recruitment are undefined. Monocyte chemoattractant protein 1 (MCP1) and macrophage inflammatory protein 2 (MIP2) are chemotactic for neutrophils in vitro and have been reported to be involved in neutrophil-dependent inflammatory tissue injury. The aim of the present study was to determine the roles of MCP1 and MIP2 in the local tissue injury induced by lung I/R.

Material and Methods
Ten large-white pigs were submitted to a left lung auto-transplant. All animals received the same anaesthetic procedure. In order to measure MCP1 and MIP2 tissue levels, lung tissue samples were taken in 4 different moments: 5 min before pneumonectomy; 5 min before reperfusion; 30 min and 60 min after reperfusion. Additionally, myeloperoxidase (MPO) content and lung oedema were also measured.

Result
Lung I/R caused substantial pulmonary damage determined as lung oedema. This oedema was accompanied by increased neutrophil accumulation (as measured by tissue MPO content, p<0.05). After 30 min of reperfusion, both MCP1 and MIP2 levels were significantly increased compared to prepneumonectomy levels (p<0.05) and a further increase was observed after 60 min reperfusion (p<0.05).

Conclusion
These results suggest that the local expression of MCP1 and MIP2 may be involved in neutrophildependent lung injury induced by I/R.