Intestinal ischemia-reperfusion injury leads to inflammatory changes in the brain.
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Intestinal ischemia-reperfusion injury leads to inflammatory changes in the brain. / Hsieh, Yu-Hsuan; McCartney, Kieran; Moore, Tyson A; Thundyil, John; Gelderblom, Mathias; Manzanero, Silvia; Arumugam, Thiruma V.
In: SHOCK, Vol. 36, No. 4, 4, 2011, p. 424-430.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Intestinal ischemia-reperfusion injury leads to inflammatory changes in the brain.
AU - Hsieh, Yu-Hsuan
AU - McCartney, Kieran
AU - Moore, Tyson A
AU - Thundyil, John
AU - Gelderblom, Mathias
AU - Manzanero, Silvia
AU - Arumugam, Thiruma V
PY - 2011
Y1 - 2011
N2 - 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-?, 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.
AB - 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-?, 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.
KW - Animals
KW - Immunohistochemistry
KW - Mice
KW - Mice, Inbred C57BL
KW - Reverse Transcriptase Polymerase Chain Reaction
KW - Immunoblotting
KW - In Situ Nick-End Labeling
KW - Tumor Necrosis Factor-alpha/metabolism
KW - Blood-Brain Barrier/metabolism
KW - Brain/immunology/metabolism
KW - Inflammation/etiology/immunology/metabolism
KW - Interleukin-6/metabolism
KW - Reperfusion Injury/complications/immunology/metabolism
KW - Animals
KW - Immunohistochemistry
KW - Mice
KW - Mice, Inbred C57BL
KW - Reverse Transcriptase Polymerase Chain Reaction
KW - Immunoblotting
KW - In Situ Nick-End Labeling
KW - Tumor Necrosis Factor-alpha/metabolism
KW - Blood-Brain Barrier/metabolism
KW - Brain/immunology/metabolism
KW - Inflammation/etiology/immunology/metabolism
KW - Interleukin-6/metabolism
KW - Reperfusion Injury/complications/immunology/metabolism
M3 - SCORING: Journal article
VL - 36
SP - 424
EP - 430
JO - SHOCK
JF - SHOCK
SN - 1073-2322
IS - 4
M1 - 4
ER -
