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Interferon-β attenuates lung inflammation following experimental subarachnoid hemorrhage

Aneurysmal subarachnoid hemorrhage (SAH) affects relatively young people and carries a poor prognosis with a case fatality rate of 35%. One of the major systemic complications associated with SAH is acute lung injury (ALI) which occurs in up to one-third of the patients and is associated with poor o...

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Published in:Critical care (London, England) England), 2010-01, Vol.14 (4), p.R157-R157, Article R157
Main Authors: Cobelens, Pieter M, Tiebosch, Ivo A C W, Dijkhuizen, Rick M, van der Meide, Peter H, Zwartbol, René, Heijnen, Cobi J, Kesecioglu, Jozef, van den Bergh, Walter M
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creator Cobelens, Pieter M
Tiebosch, Ivo A C W
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van den Bergh, Walter M
description Aneurysmal subarachnoid hemorrhage (SAH) affects relatively young people and carries a poor prognosis with a case fatality rate of 35%. One of the major systemic complications associated with SAH is acute lung injury (ALI) which occurs in up to one-third of the patients and is associated with poor outcome. ALI in SAH may be predisposed by neurogenic pulmonary edema (NPE) and inflammatory mediators. The objective of this study was to assess the immunomodulatory effects of interferon-β (IFN-β) on inflammatory mediators in the lung after experimental SAH. Male Wistar rats were subjected to the induction of SAH by means of the endovascular filament method. Sham-animals underwent sham-surgery. Rats received IFN-β for four consecutive days starting at two hours after SAH induction. After seven days, lungs were analyzed for the expression of inflammatory markers. SAH induced the influx of neutrophils into the lung, and enhanced expression of the pulmonary adhesion molecules E-selectin, inter-cellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 compared to sham-animals. In addition, SAH increased the expression of the chemokines macrophage inflammatory protein (MIP)-1α, MIP-2, and cytokine-induced neutrophil chemoattractant (CINC)-1 in the lung. Finally, tumor necrosis factor-α (TNF-α) was significantly increased in lungs from SAH-animals compared to sham-animals. IFN-β effectively abolished the SAH-induced expression of all pro-inflammatory mediators in the lung. IFN-β strongly reduces lung inflammation after experimental SAH and may therefore be an effective drug to prevent SAH-mediated lung injury.
doi_str_mv 10.1186/cc9232
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One of the major systemic complications associated with SAH is acute lung injury (ALI) which occurs in up to one-third of the patients and is associated with poor outcome. ALI in SAH may be predisposed by neurogenic pulmonary edema (NPE) and inflammatory mediators. The objective of this study was to assess the immunomodulatory effects of interferon-β (IFN-β) on inflammatory mediators in the lung after experimental SAH. Male Wistar rats were subjected to the induction of SAH by means of the endovascular filament method. Sham-animals underwent sham-surgery. Rats received IFN-β for four consecutive days starting at two hours after SAH induction. After seven days, lungs were analyzed for the expression of inflammatory markers. SAH induced the influx of neutrophils into the lung, and enhanced expression of the pulmonary adhesion molecules E-selectin, inter-cellular adhesion molecule (ICAM)-1, and vascular cell adhesion molecule (VCAM)-1 compared to sham-animals. In addition, SAH increased the expression of the chemokines macrophage inflammatory protein (MIP)-1α, MIP-2, and cytokine-induced neutrophil chemoattractant (CINC)-1 in the lung. Finally, tumor necrosis factor-α (TNF-α) was significantly increased in lungs from SAH-animals compared to sham-animals. IFN-β effectively abolished the SAH-induced expression of all pro-inflammatory mediators in the lung. 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In addition, SAH increased the expression of the chemokines macrophage inflammatory protein (MIP)-1α, MIP-2, and cytokine-induced neutrophil chemoattractant (CINC)-1 in the lung. Finally, tumor necrosis factor-α (TNF-α) was significantly increased in lungs from SAH-animals compared to sham-animals. IFN-β effectively abolished the SAH-induced expression of all pro-inflammatory mediators in the lung. IFN-β strongly reduces lung inflammation after experimental SAH and may therefore be an effective drug to prevent SAH-mediated lung injury.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>20731855</pmid><doi>10.1186/cc9232</doi><oa>free_for_read</oa></addata></record>
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subjects Acute Lung Injury - drug therapy
Acute Lung Injury - etiology
Animals
Chemokine CCL3 - analysis
Chemokine CXCL1 - analysis
E-Selectin - analysis
Inflammation - drug therapy
Intercellular Adhesion Molecule-1 - analysis
Interferon-beta - therapeutic use
Lung - chemistry
Lung - drug effects
Lung - pathology
Male
Neutrophil Infiltration - drug effects
Rats
Rats, Wistar
Reverse Transcriptase Polymerase Chain Reaction
Subarachnoid Hemorrhage - complications
Subarachnoid Hemorrhage - drug therapy
Tumor Necrosis Factor-alpha - analysis
Vascular Cell Adhesion Molecule-1 - analysis
title Interferon-β attenuates lung inflammation following experimental subarachnoid hemorrhage
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