Interferon-beta attenuates lung inflammation following experimental subarachnoid hemorrhage
IntroductionAneurysmal 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 oedema (NPE) and inflammatory mediators. The objective of this study was to assess the immunomodulatory effects of interferon-beta (IFN-beta) on inflammatory mediators in the lung after experimental SAH.
Methods: 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-beta for 4 consecutive days starting at 2 hours after SAH induction.
After 7 days, lungs were analyzed for the expression of inflammatory markers.
Results: 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)-1alpha, MIP-2, and cytokine-induced neutrophil chemoattractant (CINC)-1 in the lung.
Finally, TNF-alpha was significantly increased in lungs from SAH-animals compared to sham-animals. IFN-beta effectively abolished the SAH-induced expression of all pro-inflammatory mediators in the lung.
Conclusions: IFN-beta strongly reduces lung inflammation after experimental SAH and may therefore be an effective drug to prevent SAH-mediated lung injury.
Author: Pieter CobelensIvo TieboschRick DijkhuizenPeter van der MeideRene ZwartbolCobi HeijnenJozef KeseciogluWalter van den Bergh
Credits/Source: Critical Care 2010, 14:R157
Published on: 2010-08-23
Copyright by the authors listed above - made available via BioMedCentral (Open Access). Please
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