Increased Intestinal Permeability in Rats Subjected to Traumatic Frontal Lobe Percussion Brain Injury

Feighery, Linda; Smyth, Aoife; Keely, Simon; Baird, Alan W.; O’Connor, William T.; Callanan, John J.; Brayden, David J.

doi:10.1097/ta.0b013e3181568d9f

Cited by 49 publications

(52 citation statements)

References 33 publications

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“…Several areas of intestinal dysfunction following TBI have been described, including stomach ulceration and gastritis (Cushing's ulcer), prolonged ileus and other motility problems, and most importantly impairment of gut barrier function (Kao et al, 1998;Feighery et al, 2008). However, the precise mechanism through which TBI leads to these gastrointestinal events is unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, gastrointestinal dysfunction is frequently observed in TBI patients, including motility abnormalities and mucosal alterations that can lead to ulceration, inflammation, and increased gut permeability (Kao et al, 1998;Hang et al, 2003). Feighery and associates have demonstrated blunting of intestinal villi and increased intestinal permeability 6 h following TBI in rat models (Feighery et al, 2008). Similarly, Hang and colleagues have also shown histopathologic changes and increased gut permeability as early as 2 h, and peaking at 24 h following TBI (Hang et al, 2003).…”

Section: Introductionmentioning

confidence: 91%

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Traumatic Brain Injury and Intestinal Dysfunction: Uncovering the Neuro-Enteric Axis

Bansal¹,

Costantini²,

Kroll³

et al. 2009

Journal of Neurotrauma

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Traumatic brain injury (TBI) can lead to several physiologic complications including gastrointestinal dysfunction. Specifically, TBI can induce an increase in intestinal permeability, which may lead to bacterial translocation, sepsis, and eventually multi-system organ failure. However, the exact mechanism of increased intestinal permeability following TBI is unknown. We hypothesized that expression of tight junction protein ZO-1 and occludin, responsible for intestinal architectural and functional integrity, will decrease following TBI and increase intestinal permeability. BALB=c mice underwent a weight drop TBI model following anesthesia. Brain injury was confirmed by a neurologic assessment and gross brain pathology. Six hours following injury, FITC-dextran (25 mg 4.4 kDa FITC-dextran) was injected into the intact lumen of the isolated ileum. Intestinal permeability was measured in plasma 30 min following injection, by using spectrophotometry to determine plasma FITC-dextran concentrations. Whole ileum extracts were used to measure expression of tight junction proteins ZO-1 and occludin by Western blot. TBI caused a significant increase in intestinal permeability (110.0 mg=mL AE 22.2) compared to sham animals (29.4 mg=mL AE 9.7) 6 h after injury ( p ¼ 0.016). Expression of ZO-1 was decreased by 49% relative to sham animals ( p < 0.02), whereas expression of occludin was decreased by 73% relative to sham animals ( p < 0.001). An increase in intestinal permeability corresponds with decreased expression of tight junction proteins ZO-1 and occludin following TBI. Expression of intestinal tight junction proteins may be an important factor in gastrointestinal dysfunction following brain injury.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 91%

Traumatic Brain Injury and Intestinal Dysfunction: Uncovering the Neuro-Enteric Axis

Bansal¹,

Costantini²,

Kroll³

et al. 2009

Journal of Neurotrauma

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“…Patients manifesting post-TBI GI dysfunction have increased morbidity and longer periods of hospitalization; therefore, treatment modalities targeting prevention of GI dysfunction have important clinical implications (Cook et al, 2008;Kemp et al, 2008). Previously, we, along with others, have shown, in a mouse model, that TBI causes GI dysfunction characterized by increased intestinal permeability and marked mucosal injury, which was confirmed by intestinal histology Feighery et al, 2008;Hang et al, 2003). Furthermore, expression of the intestinal tight junction proteins, ZO-1 and occludin, decrease following TBI, which may explain, at least in part, the observed increase in intestinal permeability .…”

mentioning

confidence: 90%

The Hormone Ghrelin Prevents Traumatic Brain Injury Induced Intestinal Dysfunction

Bansal

Ryu

Blow

et al. 2010

Journal of Neurotrauma

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Intestinal barrier breakdown following traumatic brain injury (TBI) is characterized by increased intestinal permeability, leading to bacterial translocation, and inflammation. The hormone ghrelin may prevent intestinal injury and have anti-inflammatory properties. We hypothesized that exogenous ghrelin prevents intestinal injury following TBI. A weight-drop model created severe TBI in three groups of anesthetized Balb/c mice. Group TBI: animals underwent TBI only; Group TBI/ghrelin: animals were given 10 mg of ghrelin intraperitoneally prior and 1 h following TBI; Group sham: no TBI or ghrelin injection. Intestinal permeability was measured 6 h following TBI by detecting serum levels of FITC-Dextran after injection into the intact ileum. The terminal ileum was harvested for histology, expression of the tight junction protein MLCK and inflammatory cytokine TNF-a. Permeability increased in the TBI group compared to the sham group (109.7 AE 21.8 mg/mL vs. 32.2 AE 10.1 mg/mL; p < 0.002). Ghrelin prevented TBI-induced permeability (28.3 AE 4.2 mg/mL vs. 109.7 AE 21.8 mg/mL; p < 0.001). The intestines of the TBI group showed blunting and necrosis of villi compared to the sham group, while ghrelin injection preserved intestinal architecture. Intestinal MLCK increased 73% compared to the sham group ( p < 0.03). Ghrelin prevented TBI-induced MLCK expression to sham levels. Intestinal TNF-a increased following TBI compared to the sham group (46.2 AE 7.1 pg/mL vs. 24.4 AE 2.2 pg/mL p < 0.001). Ghrelin reduced TNF-a to sham levels (29.2 AE 5.0 pg/mL; p ¼ NS). We therefore conclude that ghrelin prevents TBI-induced injury, as determined by intestinal permeability, histology, and intestinal levels of TNF-a. The mechanism for ghrelin mediating intestinal protection is likely multifactorial, and further studies are needed to delineate these possibilities.

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“…The majority of patients with temperate to severe TBI have upper GI intolerance in the first few weeks after injury [31,32]. Feighery et al have demonstrated blunting of intestinal villi and increased intestinal permeability, 6 h following TBI in rats [23] (Fig. 1).…”

Section: Tbi and Gi Problemsmentioning

confidence: 99%

“…stomach ulceration and gastritis (Cushing's ulcer), prolonged ileus and other motility problems) and most significantly, impairment of gut barrier function [9,23]. GI dysfunction frequently occurs in patients with TBI and some GI tract disorders experienced during acute stages of stroke are usually considered as stressinduced injuries [24].…”

Section: Tbi and Gi Problemsmentioning

confidence: 99%

Traumatic Brain Injury and the Gastrointestinal Tract: The Role of Female Sexual Hormones

et al. 2017

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Traumatic brain injury (TBI) is an important public health problem which can lead to several complications like gastrointestinal dysfunction. Patients with TBI often suffer from gastrointestinal dysfunctions such as enteral feeding intolerance. Gastric ulceration is induced by various forms of stress like surgery, ischemia and trauma. TBI causes a delayed but significant decrease in intestinal contractile activity in the ileum leading to delayed transport. The association between severity of brain injury and enteral feeding intolerance suggests a strong link between the central nervous system and the non-functional gut. The results of recent basic and clinical studies revealed the beneficial effects of estrogen and progesterone hormones in the treatment of gastrointestinal dysfunction. Females have more resistance to stress and fewer gastrointestinal lesions occur in females as compared to males. Sex steroid hormones have sparked interest as possible neuroprotective agents after traumatic injury and many studies have been done on this subject. This article reviews the literature related to some possible physiological effects of female sexual hormones on the gastrointestinal tract following TBI.

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Increased Intestinal Permeability in Rats Subjected to Traumatic Frontal Lobe Percussion Brain Injury

Cited by 49 publications

References 33 publications

Traumatic Brain Injury and Intestinal Dysfunction: Uncovering the Neuro-Enteric Axis

Traumatic Brain Injury and Intestinal Dysfunction: Uncovering the Neuro-Enteric Axis

The Hormone Ghrelin Prevents Traumatic Brain Injury Induced Intestinal Dysfunction

Traumatic Brain Injury and the Gastrointestinal Tract: The Role of Female Sexual Hormones

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