Mechanisms of postburn intestinal barrier dysfunction in the rat: Roles of epithelial cell renewal, E-cadherin, and neutrophil extravasation*

Al-Ghoul, Walid M.; Khan, M.; Fazal, Nadeem; Sayeed, M. M.

doi:10.1097/01.ccm.0000132896.62368.01

Cited by 31 publications

(26 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neutrophils seems to play a central role in burn injury-induced intestinal barrier dysfunction by means of the release of superoxide anion, among other pro-inflammatory molecules [146,148]. Nevertheless, the mechanisms implicated in neutrophil infiltration of the gastrointestinal tract after stress are largely unknown and remains subject of future research.…”

Section: Neutrophilsmentioning

confidence: 99%

The Effects of Physical and Psychological Stress on the Gastrointestinal Tract: Lessons from Animal Models

Caso

Leza²,

Menchén³

2008

CMM

113

View full text Add to dashboard Cite

Physical and psychological stresses are widely accepted as triggers and / or modifiers of the clinical course of diverse gastrointestinal disorders such as peptic ulcer, irritable bowel syndrome or inflammatory bowel disease. Growing experimental evidence from a variety of models such as immobilization, thermal injury or early maternal deprivation in laboratory animals uniformly supports the ability of stress to induce the development of gastric ulcers, altered gastrointestinal motility and ion secretion, and increased intestinal permeability leading to the passage of antigens to the lamina propria and bacterial translocation. Stress can also synergize with other pathogenic factors such as Helicobacter pylori, non-steroidal anti-inflammatory drugs or colitis-inducing chemicals to produce gastrointestinal disease. The brain-gut axis provides the anatomical basis through emotions and environmental influences modulate the gastrointestinal function through the regulation of gastrointestinal immune system and mucosal inflammation; in this sense, mucosal mast cells - at cellular level - and corticotropin releasing factor (CRF) - at molecular level - seem to play a crucial role. On the other hand, an array of adaptive responses have been evolved in order to maintain the homeostasis and to ensure the survival of the individual. In the gut mucosa anti-inflammatory pathways counteract the deleterious effect of the stressful stimuli on the gastrointestinal homeostasis. In the present review we discuss the several experimental approaches used to mimic human stressful events or chronic stress in laboratory animals, the evidence of stress-induced gastrointestinal inflammation and dysfunction derived from them, and the involved cellular and molecular mechanisms that are being discovered during the last years.

show abstract

Section: Neutrophilsmentioning

confidence: 99%

The Effects of Physical and Psychological Stress on the Gastrointestinal Tract: Lessons from Animal Models

Caso

Leza²,

Menchén³

2008

CMM

113

View full text Add to dashboard Cite

show abstract

“…However, deeper or more extensive injuries stimulate changes that would affect most, if not all, body systems including the gut. The pathophysiologic events following thermal injuries consist in the neutrophil influx with extravasation in the lamina propria (postburn day 1), increased intestinal myeloperoxidase activity (postburn day 3), decreased epithelial cell proliferation, migration, and E-cadherin expression (postburn day 3), increased E. Faecalis bacterial translocation (postburn day 3) [1] and massive necrosis and apoptosis [2]. Gut mucosal apoptosis following thermal burns was first investigated and described in 1999 by Wolf et al and by Lightfood et al [3,4].…”

Section: Gutmentioning

confidence: 99%

“Systemic apoptotic response” after thermal burns

Gravante

Delogu

Sconocchia³

2006

Apoptosis

View full text Add to dashboard Cite

The systemic pathophysiologic changes following thermal injuries affect multiple organs and body systems leading to clinical manifestations including shock, intestinal alterations, respiratory and renal failure, immunosuppression and others. Recent advances in the comprehension of mechanisms underlying systemic complications of thermal injuries have contributed to uncover part of the cellular and molecular basis that underlie such changes. Recently, programmed cell death (apoptosis) has been considered playing an important role in the development of such pathological events. Therefore, investigators utilizing animal models and clinical studies involving human primates have produced a large body of information suggesting that apoptosis is associated with most of the tissue damages triggered by severe thermal injuries. In order to draw the attention on the important role of apoptosis on systemic complications of thermal injuries, in this review we describe most of these studies, discuss possible cellular and molecular mechanisms and indicate ways to utilize them for the development of therapeutic strategies by which apoptosis may be prevented or counteracted.

show abstract

“…Much of this damage can be limited by depletion of neutrophils prior to injury (14). The rise in neutrophils correlates with a decrease in E-cadherin expression, increased epithelial cell apoptosis, and decreased epithelial cell proliferation (15). Taken together, these changes diminish intestinal barrier function and make victims susceptible to bacterial translocation and subsequent death due to sepsis.…”

Section: Introductionmentioning

confidence: 99%

Neutrophil Accumulation in the Small Intestine Contributes to Local Tissue Destruction Following Combined Radiation and Burn Injury

Carter

Chen

Palmer

et al. 2016

Journal of Burn Care & Research

View full text Add to dashboard Cite

Objective The threat of nuclear disaster makes combined radiation and thermal burn injury (CRI) a relevant topic when discussing modern trauma, as burn injuries are likely to occur with detonation of a conventional nuclear weapon. Previous studies in a murine model have shown that there is a breakdown of the gut epithelium and subsequent bacterial translocation into mesenteric lymph nodes after CRI. This study examines the early innate immune response of the small intestine following CRI. Methods Using a previously established murine model of 5 - 5.5Gy total body irradiation combined with 15% total body surface area burn, the injury response of the small intestine was examined at 24, 48 and 72hr by visual assessment, myeloperoxidase and cytokine measurement. Results At 24hr, intestinal damage as measured by villus blunting, crypt debris and decreased mitosis, was apparent in all injury groups but the derangements persisted out to 72hr only with CRI. The prolonged intestinal damage in CRI was accompanied by a 2-fold (p<0.05) elevation in myeloperoxidase activity over sham animals at 48hr and persisted as a 3-fold (p<0.05) elevation at 72hr post-injury. Corresponding levels of KC were 8-fold (p<0.05) higher than sham at 48hr with persistent elevation at 72hr. Conclusions An enhanced innate immune response, partially mediated by the influx of neutrophils into the gastrointestinal tract is contributing to the hyperinflammatory state seen following CRI. Attenuation of the local gastrointestinal inflammatory response may play a major role in managing victims following nuclear disaster.

show abstract

Mechanisms of postburn intestinal barrier dysfunction in the rat: Roles of epithelial cell renewal, E-cadherin, and neutrophil extravasation*

Cited by 31 publications

References 57 publications

The Effects of Physical and Psychological Stress on the Gastrointestinal Tract: Lessons from Animal Models

The Effects of Physical and Psychological Stress on the Gastrointestinal Tract: Lessons from Animal Models

“Systemic apoptotic response” after thermal burns

Neutrophil Accumulation in the Small Intestine Contributes to Local Tissue Destruction Following Combined Radiation and Burn Injury

Contact Info

Product

Resources

About