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1 Department of Cell and Molecular Biology, University of Rhode Island, Kingston, RI, USA
2 Department of Surgery, Rhode Island Hospital and Brown University School of Medicine, Providence, RI, USA
* To whom correspondence should be addressed. E-mail: aayala{at}lifespan.org.
Acute lung injury (ALI) is identified with the targeting/sequestration of PMN to the lung. Instrumental to PMN targeting are chemokines (eg. MIP-2, KC, etc.) produced by macrophage, PMN and other resident pulmonary cells. However, the relative contribution of resident pulmonary macrophages as opposed to PMN in inducing ALI is poorly understood. We therefore hypothesize that depletion of peripheral blood PMN and/or the oblation of a macrophage mediated PMN chemokine signal (via macrophage deficiency) will reduce the inflammation and ALI observed in mice following hemorrhage (Hem) and subsequent sepsis (CLP) in our murine model of ALI. To examine this we pretreated mice with either 500 ug anti-mouse Gr1 antibody/animal (to deplete PMN) or subjected mice deficient in mature macrophage (B6C3Fe-a/a-CsF1op) to Hem (90 minutes at 35±5mmHg) followed by resuscitation. 24 hours post Hem mice were subjected to CLP, euthanized 24 hours later and lung tissue samples collected. Our data showed that in the absence of either peripheral blood PMN or mature tissue macrophages there was a suppression of IL-6, KC, and MIP-2 levels in lung tissue from Hem/CLP mice as well as a reduction in PMN influx to the lung and lung injury (BALF protein). In contrast, lung tissue IL-10 and TNF-
levels were suppressed in the macrophage deficient Hem/CLP mice as compared to PMN depleted Hem/CLP mice. Together, these data suggest that both the PMN and the macrophage are required to induce inflammation seen here, however, macrophage not PMN regulate the release of IL-10, independent of local changes in TNF.
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