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 |
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Rok vydání: | 2011 |
Předmět: |
medicine.medical_specialty
P-selectin Immunoblotting Central nervous system Critical Care and Intensive Care Medicine Blood–brain barrier Systemic inflammation Mice Internal medicine In Situ Nick-End Labeling medicine Animals Neuroinflammation Inflammation Kidney Microglia Interleukin-6 Reverse Transcriptase Polymerase Chain Reaction Tumor Necrosis Factor-alpha business.industry Brain medicine.disease Immunohistochemistry Mice Inbred C57BL medicine.anatomical_structure Endocrinology Blood-Brain Barrier Reperfusion Injury Emergency Medicine medicine.symptom business Reperfusion injury |
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 |
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