Investigation into the signal transduction pathway via which heat stress impairs intestinal epithelial barrier function

Yang, Ping‐Chang; He, Shaoheng; Zheng, Peng‐Yuan

doi:10.1111/j.1440-1746.2006.04710.x

Cited by 78 publications

(62 citation statements)

References 41 publications

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“…Indeed, moderate temperature elevation produced a reversible decrease in TER and ZO-1 expression leading to increased paracellular permeability in the absence of cell apoptosis or necrosis [131,132]. Hyperosmotic stress induced both expression of the proinflammatory chemokine IL-8 and epithelial barrier dysfunction [133,134].…”

Section: Miscellaneousmentioning

confidence: 99%

“…Inhibition of MLCK did not prevent EPECinduced PKC-translocation or activation, suggesting that PKC-controlled epithelial barrier through a distinct or upstream signalling pathway. As regards heat stress, intestinal epithelial barrier dysfunction was due to subsequent phosphorylation and activation of PKC and MLCK leading to upregulation of MLC phosphorylation [132].…”

Section: Inhibition Of Mlck An Enzyme Activated By Several Stimulimentioning

confidence: 99%

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Intestinal Epithelial Barrier Dysfunction in Disease and Possible Therapeutical Interventions

Catalioto

Maggi²,

Giuliani³

2011

CMC

143

102

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The intestinal epithelial monolayer constitutes a physical and functional barrier between the organism and the external environment. It regulates nutrients absorption, water and ion fluxes, and represents the first defensive barrier against toxins and enteric pathogens. Epithelial cells are linked together at the apical junctional complex by tight junctions that reduce the extracellular space and the passage of charge entities while forming a physical barrier to lipophilic molecules. Cultured intestinal epithelial cells have been extensively used to study intestinal absorption of newly synthesized drugs and the regulation of tight junctions structure and function. In vitro mild irritants, proinflammatory cytokines, toxins and pathogens, and adverse environmental conditions open tight junctions and increase paracellular permeability, an effect often accompanied by immune activation of the enterocytes. Conversely, inhibition of proinflammatory cytokines, exposure to growth factors and probiotics, among others, exert a protective effect. Impaired barrier function results from activation of signalling pathways that lead to alteration of junctional proteins expression and/or distribution. In vivo, intestinal barrier dysfunction is associated with various intestinal and non-intestinal disorders including inflammatory bowel disease, celiac disease, and diarrhoeal infection. This review will describe the current knowledge of the mechanisms regulating tight junctions and intestinal permeability, how these findings have lead to a better understanding of barrier alteration in human intestinal disorders, and what the emerging therapies to treat these pathologies are.

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Section: Miscellaneousmentioning

confidence: 99%

Section: Inhibition Of Mlck An Enzyme Activated By Several Stimulimentioning

confidence: 99%

Intestinal Epithelial Barrier Dysfunction in Disease and Possible Therapeutical Interventions

Catalioto

Maggi²,

Giuliani³

2011

CMC

143

102

View full text Add to dashboard Cite

show abstract

“…51 Even exogenous HSP70 added to cell cultures was able to prevent the heat stress-induced alteration in permeability. 52 HSP70 was recently shown to be redistributed at the cytoskeleton level following Caco2 cell exposure to wheat gliadin, which induced cytoskeletal alterations, thus strengthening further the role of HSP70 in the maintenance of barrier function. 53 Heat stress augmented the expression of HSP70 and occludin, thus probably limiting ileal permeability alterations in pigs.…”

Section: Gut Barrier Functionmentioning

confidence: 99%

Gut epithelial inducible heat-shock proteins and their modulation by diet and the microbiota

Arnal

Lallès

2016

Nutr Rev

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“…In addition, both heatinduced injury to the epithelial lining (22) and regulated opening of epithelial tight junctions (11,47) have been implicated as important underlying mechanisms of increased permeability.…”

mentioning

confidence: 99%

Hyperthermia induces injury to the intestinal mucosa in the mouse: evidence for an oxidative stress mechanism

Oliver

Phillips

Novosad

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Loss of the intestinal barrier is critical to the clinical course of heat illness, but the underlying mechanisms are still poorly understood. We tested the hypothesis that conditions characteristic of mild heatstroke in mice are associated with injury to the epithelial lining of the intestinal tract and comprise a critical component of barrier dysfunction. Anesthetized mice were gavaged with 4 kDa FITC-dextran (FD-4) and exposed to increasing core temperatures, briefly reaching 42.4°C, followed by 30 min recovery. Arterial samples were collected to measure FD-4 concentration in plasma (in vivo gastrointestinal permeability). The small intestines were then removed to measure histological evidence of injury. Hyperthermia resulted in a ≈2.5-fold elevation in plasma FD-4 and was always associated with significant histological evidence of injury to the epithelial lining compared with matched controls, particularly in the duodenum. When isolated intestinal segments from control animals were exposed to ≥41.5°C, marked increases in permeability were observed within 60 min. These changes were associated with release of lactate dehydrogenase, evidence of protein oxidation via carbonyl formation and histological damage. Coincubation with N-acetylcysteine protected in vitro permeability during hyperthermia and reduced histological damage and protein oxidation. Chelation of intracellular Ca(2+) to block tight junction opening during 41.5°C exposure failed to reduce the permeability of in vitro segments. The results demonstrate that hyperthermia exposure in mouse intestine, at temperatures at or below those necessary to induce mild heatstroke, cause rapid and substantial injury to the intestinal lining that may be attributed, in part, to oxidative stress.

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Investigation into the signal transduction pathway via which heat stress impairs intestinal epithelial barrier function

Abstract: Heat stress can induce intestinal epithelial barrier dysfunction via the PKC and MLC signal transduction pathway.

Cited by 78 publications

References 41 publications

Intestinal Epithelial Barrier Dysfunction in Disease and Possible Therapeutical Interventions

Intestinal Epithelial Barrier Dysfunction in Disease and Possible Therapeutical Interventions

Gut epithelial inducible heat-shock proteins and their modulation by diet and the microbiota

Hyperthermia induces injury to the intestinal mucosa in the mouse: evidence for an oxidative stress mechanism

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