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Activation of alveolar macrophages in lung injury associated with experimental acute pancreatitis is mediated by the liver

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dc.creator Closa, Daniel
dc.creator Sabater, Luis
dc.creator Fernández Cruz, Laureano
dc.creator Prats, Neus
dc.creator Gelpí, Emili
dc.creator Roselló-Catafau, Joan
dc.date 2008-02-18T15:52:15Z
dc.date 2008-02-18T15:52:15Z
dc.date 1999-02
dc.date.accessioned 2017-01-31T01:00:10Z
dc.date.available 2017-01-31T01:00:10Z
dc.identifier Annals of Surgery 229(2): 230-236 (1999)
dc.identifier 0003-4932
dc.identifier http://hdl.handle.net/10261/2965
dc.identifier 10.1097/00000658-199902000-00011
dc.identifier.uri http://dspace.mediu.edu.my:8181/xmlui/handle/10261/2965
dc.description [OBJECTIVE] To evaluate (1) whether alveolar macrophages are activated as a consequence of acute pancreatitis (AP), (2) the implication of inflammatory factors released by these macrophages in the process of neutrophil migration into the lungs observed in lung injury induced by AP, and (3) the role of the liver in the activation of alveolar macrophages.
dc.description [SUMMARY BACKGROUND DATA] Acute lung injury is the extrapancreatic complication most frequently associated with death and complications in severe AP. Neutrophil infiltration into the lungs seems to be related to the release of systemic and local mediators. The liver and alveolar macrophages are sources of mediators that have been suggested to participate in the lung damage associated with AP.
dc.description [METHODS] Pancreatitis was induced in rats by intraductal administration of 5% sodium taurocholate. The inflammatory process in the lung and the activation of alveolar macrophages were investigated in animals with and without portocaval shunting 3 hours after AP induction. Alveolar macrophages were obtained by bronchoalveolar lavage. The generation of nitric oxide, leukotriene B4, tumor necrosis factor-alpha, and MIP-2 by alveolar macrophages and the chemotactic activity of supernatants of cultured macrophages were evaluated.
dc.description [RESULTS] Pancreatitis was associated with increased infiltration of neutrophils into the lungs 3 hours after induction. This effect was prevented by the portocaval shunt. Alveolar macrophages obtained after induction of pancreatitis generated increased levels of nitric oxide, tumor necrosis factor-alpha, and MIP-2, but not leukotriene B4. In addition, supernatants of these macrophages exhibited a chemotactic activity for neutrophils when instilled into the lungs of unmanipulated animals. All these effects were abolished when portocaval shunting was carried out before induction of pancreatitis.
dc.description [CONCLUSION] Lung damage induced by experimental AP is associated with alveolar macrophage activation. The liver mediates the alveolar macrophage activation in this experimental model.
dc.description Supported by 1996 Research Grant Program of the Hospital Clinic, University of Barcelona.
dc.description Peer reviewed
dc.format 68416 bytes
dc.format 1830730 bytes
dc.format image/jpeg
dc.format application/pdf
dc.language eng
dc.publisher Lippincott Williams & Wilkins
dc.relation http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1191636
dc.relation http://dx.doi.org/10.1097/00000658-199902000-00011
dc.rights openAccess
dc.subject Acute Pancreatitis
dc.subject Lung injury
dc.subject Alveolar Macrophages
dc.subject Liver
dc.title Activation of alveolar macrophages in lung injury associated with experimental acute pancreatitis is mediated by the liver
dc.type Artículo


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