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4 results on '"Hadenque A"'

1. In vivo evidence for the role of GM-CSF as a mediator in acute pancreatitis-associated lung injury

Author

Frossard, Jean Louis, Saluja, Ashok K., Mach, Nicolas, Lee, Hong Sik, Bhagat, Lakshmi, Hadenque, Antoine, Rubbia-Brandt, Laura, Dranoff, Glenn, and Steer, Michael L.

Subjects
Molecular biology -- Research, Granulocyte-macrophage colony stimulating factor -- Physiological aspects, Pancreatitis -- Physiological aspects, Lungs -- Physiological aspects, Respiratory distress syndrome -- Physiological aspects, Inflammation -- Physiological aspects, Cell adhesion molecules -- Physiological aspects, Neutrophils -- Physiological aspects, Mice, mutant strains -- Physiological aspects, Biological sciences
Abstract

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 experimental pancreatitis was evaluated with GM-CSF knockout mice (GM-CSF -/-). Pancreatitis was induced by hourly (12x) intraperitoneal injection of a supramaximally stimulating dose of the cholecystokinin analog 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 ALI and suggest that GM-CSF may act indirectly by regulating the release of other proinflammatory factors including MIP-2. granulocyte-macrophage colony-stimulating factor; caerulein; inflammation; adult respiratory distress syndrome; adhesion molecules; neutrophils

Published
2002

2. In vivo evidence for the role of GM-CSF as a mediator in acute pancreatitis-associated lung injury

Author

Lakshmi Bhagat, Hong Sik Lee, Michael L. Steer, Glenn Dranoff, Antoine Hadenque, Nicolas Mach, Laura Rubbia-Brandt, Jean Louis Frossard, and Ashok K. Saluja

Subjects
Pulmonary and Respiratory Medicine, Lung Diseases, Pancreatic disease, Physiology, Chemokine CXCL2, Lung injury, Severity of Illness Index, Antibodies, Leukocyte Count, Mice, Reference Values, Physiology (medical), medicine, Animals, Respiratory system, Lung, Pancreas, Mice, Knockout, Respiratory distress, business.industry, Respiratory disease, Granulocyte-Macrophage Colony-Stimulating Factor, Cell Biology, respiratory system, medicine.disease, respiratory tract diseases, medicine.anatomical_structure, Pancreatitis, Immunology, Acute Disease, Acute pancreatitis, Chemokines, business, Ceruletide
Abstract

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 experimental pancreatitis was evaluated with GM-CSF knockout mice (GM-CSF −/−). Pancreatitis was induced by hourly (12×) intraperitoneal injection of a supramaximally stimulating dose of the cholecystokinin analog 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 ALI and suggest that GM-CSF may act indirectly by regulating the release of other proinflammatory factors including MIP-2.

Published
2002

3. Providing scientific evidence: RCTs and beyond

Author

Sørensen, Thorkild I.A., Hadenque, A, Salerno, F, Bendtsen, F, Talwalkar, J, Heathcote, J, Blei, A.T.,Rodés,J, Franchis, R de, Sørensen, Thorkild I.A., Hadenque, A, Salerno, F, Bendtsen, F, Talwalkar, J, Heathcote, J, Blei, A.T.,Rodés,J, and Franchis, R de

Published
2006

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