Enhanced pulmonary inflammation following experimental intracerebral hemorrhage

The association between brain damage and respiratory dysfunction has been recognized although mechanistic link between the two is still poorly defined. Intracerebral hemorrhage is accompanied by brain injury, stroke, and parenchymal hematoma formation with surrounding inflammation. Increase intracranial pressure as a result of intracerebral hemorrhage may promote localized activation of cytokines and coagulation system including tissue factor release. However, whether intracerebral hemorrhage triggers inflammation in noncerebral organs has not been elucidated. The aim of the present study was to examine the impact of intracerebral hemorrhage on lung inflammatory response. Intracerebral hemorrhage was induced by stereotaxic intrastriatal administration of bacterial collagenase. Expression of intracellular adhesion molecule-1 (ICAM-1), IKB-alpha, tissue factor, tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) was evaluated by Western blot analysis. Our results revealed that intracerebral hemorrhage upregulated expression of ICAM-1 and tissue factor in both brain and lung, whereas it enhanced TNF-alpha and IL-1beta mainly in brain within 6 and 24 h of the brain injury. Levels of IKB-alpha remained unchanged in brain and lung tissues. Appearance of inflammatory markers in the lung was accompanied by morphological pulmonary damage. These data suggest that intracerebral hemorrhage may trigger acute inflammatory response in both brain and lung.