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Articles in PresS, published online ahead of print May 3, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00413.2001
Submitted on October 23, 2001
Accepted on April 4, 2002
1 Department of Surgery, Harvard Medical School & Beth Israel Deaconess Medical Center, Boston, MA, USA; Division of Gastroenterology, Geneva University Hospitals, Geneva, Switzerland
2 Department of Surgery, Harvard Medical School & Beth Israel Deaconess Medical Center, Boston, MA, USA
3 Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA, USA; Division of Oncology, Geneva University Hospitals, Geneva, Switzerland
4 Division of Clinical Pathology, Geneva University Hospitals, Geneva, Switzerland
5 Division of Gastroenterology, Geneva University Hospitals, Geneva, Switzerland
6 Department of Adult Oncology, Dana-Farber Cancer Institute, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: msteer{at}bidmc.harvard.edu.
Severe pancreatitis is frequently associated with acute lung injury (ALI) and the respiratory distress syndrome. The role of granulocyte-macrophage colony stimulating factor (GM-CSF) in mediating the ALI associated with secretagogue-induced pancreatitis was evaluated using GM-CSF knockout mice (GM-CSF -/-). Pancreatitis was induced by hourly (X12) intraperitoneal injection of a supramaximally stimulating dose of caerulein. The resulting pancreatitis was similar in GM-CSF sufficient (GM-CSF +/+) control animals and GM-CSF -/- mice. Lung injury, quantitated by measuring lung myeloperoxidase activity (an indicator of neutrophil sequestration), alveolar-capillary permeability, and alveolar membrane thickness was less severe in GM-CSF -/- than in GM-CSF +/+ mice. In GM-CSF+/+ mice, pancreas, lung and serum GM-CSF levels increase during pancreatitis. Lung levels of macrophage inflammatory protein(MIP-2) are also increased during pancreatitis but, in this case, the rise is less profound in GM-CSF -/- mice than in GM-CSF +/+ controls. Administration of anti-MIP-2 antibodies was found to reduce the severity of pancreatitis-associated ALI. Our findings indicate that GM-CSF plays a critical role in coupling pancreatitis to acute lung injury and they suggest that GM-CSF may act indirectly by regulating the release of other pro-inflammatory factors including MIP-2.
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