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This Article Full Text Full Text (PDF) All Versions of this Article: 296/4/R979    most recent 90825.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Caso, J. R. Articles by Leza, J. C. Search for Related Content PubMed PubMed Citation Articles by Caso, J. R. Articles by Leza, J. C.

INFLAMMATION, CYTOKINES, NEUROIMMUNE INTERACTIONS

Colonic bacterial translocation as a possible factor in stress-worsening experimental stroke outcome

Faculty of Medicine, Departments of ¹Pharmacology and ³Microbiology I, University Complutense, Madrid; ²Servicio de Aparato Digestivo, Hospital General Universitario "Gregorio Marañon" and CIBEREHD, Madrid; and ⁴Centro de Investigación Biomédica en Red de Salud Mental, CIBERSAM, Madrid, Spain

Submitted 10 October 2008 ; accepted in final form 27 January 2009

Stress is known to be one of the risk factors of stroke, but only a few experimental studies have examined the possible mechanisms by which prior stress may affect stroke outcome. In stroke patients, infections impede neurological recovery and increase morbidity as well as mortality. We previously reported that stress induces a bacterial translocation and that prior immobilization stress worsens experimental stroke outcome through mechanisms that involve inflammatory mediators such as release of proinflammatory cytokines and enzyme activation. We now investigate whether bacterial translocation from the intestinal flora of rats with stress before experimental ischemia is involved in stroke outcome. We used an experimental paradigm consisting of exposure of Fischer rats to repeated immobilization sessions before permanent middle cerebral artery occlusion (MCAO). The presence of bacteria and the levels and expression of different mediators involved in the bacterial translocation were analyzed. Our results indicate that stress before stroke is related to the presence of bacteria in different organs (mesenteric nodes, spleen, liver, and lung) after MCAO and increases inflammatory colonic parameters (such as cyclooxygenase-2, inducible nitric oxide synthase, and myeloperoxidase), but decreases colonic immunoglobulin A, and these results are correlated with colonic inflammation and bacterial translocation. Understanding the implication of bacterial translocation during stress-induced stroke worsening is of great potential clinical relevance, given the high incidence of infections after severe stroke and their main role in mortality and morbidity in stroke patients.

stress; stroke; bacterial translocation; intestinal barrier; stroke outcome