Intestinal Ischemia-Reperfusion Injury Leads to Inflammatory Changes in the Brain

Autor: Kieran McCartney, Tyson A. Moore, John Thundyil, Silvia Manzanero, Thiruma V. Arumugam, Mathias Gelderblom, Yu-Hsuan Hsieh
Rok vydání: 2011
Předmět:
Zdroj: Shock. 36:424-430
ISSN: 1073-2322
DOI: 10.1097/shk.0b013e3182295f91
Popis: Intestinal ischemia-reperfusion (I/R) injury is a well-established animal model of systemic inflammation and can lead to multiple organ failure as well as severe and lasting morbidity and even death. It can occur in humans as a result of vascular surgery or as secondary sequelae to many common conditions including low blood pressure, myocardial infarction, and necrotizing enterocolitis. Systemic inflammation induced through kidney I/R injury has been shown previously to lead to encephalopathic adverse effects, and it was theorized that intestinal injury would also cause secondary central nervous system effects. This study presents evidence that over a 6-h time frame, mouse intestinal I/R injury does not cause neuronal cell death in the brain in vivo. However, at the genetic level, certain inflammatory mediators such as endothelial nitric oxide synthase, intercellular adhesion molecule 1, P selectin, TNF-α, and IL-6 are significantly upregulated. There was a significant increase in brain edema observed in sham-operated animals as well as in fasted and nonfasted I/R groups, but neurons were not apoptotic, in the 6-h time period. Conversely, Iba1-expressing activated microglia cells and glial fibrillary acidic protein-expressing astrocytes were found to be markedly increased in fasted and nonfasted I/R mice compared with controls and sham-operated animals. These data demonstrate that intestinal I/R injury induces inflammatory changes in the brain.
Databáze: OpenAIRE