Sarah J Spencer1, Abdeslam Mouihate, Quentin J Pittman. 1. Hotchkiss Brain Institute and Institute of Infection, Immunity and Inflammation, Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada. spences@ucalgary.ca
Abstract
BACKGROUND AND PURPOSE: Concomitant infection can exacerbate damage caused by cerebral ischemia. However, the interaction between and relative importance of the febrile and inflammatory components of the immune response is still unknown. METHODS: Male Sprague-Dawley rats were subjected to a 2-vessel occlusion with hypotension, immediately followed by intraperitoneal injection of lipopolysaccharide or pyrogen-free saline. RESULTS: Inflammation immediately after 2-vessel occlusion exacerbated hippocampal cell loss at 3 days and enhanced anxiety-related behaviors in the elevated plus maze and open field. These effects were not associated with differences in body temperature changes or with hippocampal pro-inflammatory cytokine production or hippocampal microglial activation. CONCLUSIONS: We show a previously undocumented dissociation between lipopolysaccharide-exacerbated damage after global ischemia in the rat and the temperature and acute brain immune response, indicating that the mechanism for enhanced lipopolysaccharide damage is hippocampal cytokine and temperature independent in this case.
BACKGROUND AND PURPOSE: Concomitant infection can exacerbate damage caused by cerebral ischemia. However, the interaction between and relative importance of the febrile and inflammatory components of the immune response is still unknown. METHODS: Male Sprague-Dawley rats were subjected to a 2-vessel occlusion with hypotension, immediately followed by intraperitoneal injection of lipopolysaccharide or pyrogen-free saline. RESULTS:Inflammation immediately after 2-vessel occlusion exacerbated hippocampal cell loss at 3 days and enhanced anxiety-related behaviors in the elevated plus maze and open field. These effects were not associated with differences in body temperature changes or with hippocampal pro-inflammatory cytokine production or hippocampal microglial activation. CONCLUSIONS: We show a previously undocumented dissociation between lipopolysaccharide-exacerbated damage after global ischemia in the rat and the temperature and acute brain immune response, indicating that the mechanism for enhanced lipopolysaccharide damage is hippocampal cytokine and temperature independent in this case.
Authors: Greg J Norman; John S Morris; Kate Karelina; Zachary M Weil; Ning Zhang; Yousef Al-Abed; Holly M Brothers; Gary L Wenk; Valentin A Pavlov; Kevin J Tracey; A Courtney Devries Journal: J Neurosci Date: 2011-03-02 Impact factor: 6.167
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