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Abstract
BackgroundInfections related to stroke-induced immunodepression are an important complication causing a high rate of death in patients. Several experimental studies in mouse stroke models have described this process but it has never been tested in other species such as rats.MethodsOur study focused on the appearance of secondary systemic and pulmonary infections in ischemic rats, comparing with sham and naive animals. For that purpose, male Wistar rats were subjected to embolic middle cerebral artery occlusion (eMCAO) or to transient MCAO (tMCAO) inserting a nylon filament. Forty-eight hours after ischemia, blood and lung samples were evaluated.ResultsIn eMCAO set, ischemic rats showed a significant decrease in blood-peripheral lymphocytes (naive = 58.8±18.1%, ischemic = 22.9±16.4%) together with an increase in polymorphonuclears (PMNs) (naive = 29.2±14.7%, ischemic = 71.7±19.5%), while no change in monocytes was observed. The increase in PMNs counts was positively correlated with worse neurological outcome 48 hours after eMCAO (r = 0.55, p = 0.043). However, sham animals showed similar changes in peripheral leukocytes as those seen in ischemic rats (lymphocytes: 40.1±19.7%; PMNs: 51.7±19.2%). Analysis of bacteriological lung growth showed clear differences between naive (0±0 CFU/mL; log10) and both sham (3.9±2.5 CFU/mL; log10) and ischemic (4.3±2.9 CFU/mL; log10) groups. Additionally, naive animals presented non-pathological lung histology, while both sham and ischemic showed congestion, edema or hemorrhage. Concordant results were found in the second set of animals submitted to a tMCAO.ConclusionsInflammatory and infection changes in Wistar rats subjected to MCAO models may be attributed not only to the brain ischemic injury but to the surgical aggression and/or anaesthetic stress. Consequently, we suggest that stroke-induced immunodepression in ischemic experimental models should be interpreted with caution in further experimental and translational studies, at least in rat stroke models that entail cervicotomy and cranial trepanation.
Highlights
Stroke produces local brain injury and causes a systemic inflammatory response followed by an immunodepression process which predisposes patients to infections
This immunodepression state is thought to be induced through a sympathetic nervous system over-action which contributes to an increase of catecholamines and glucocortocoids [1]
Changes in peripheral leukocytes count are correlated with neurological outcome after stroke
Summary
Stroke produces local brain injury and causes a systemic inflammatory response followed by an immunodepression process which predisposes patients to infections. This immunodepression state is thought to be induced through a sympathetic nervous system over-action which contributes to an increase of catecholamines and glucocortocoids [1]. The incidence and prognostic impact of infections have been recently evaluated in a meta-analysis on this subject, which concluded that infections complicated acute stroke in 30% of patients [3]. Several experimental studies in mouse stroke models have described this process but it has never been tested in other species such as rats
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