Intestinal inflammation and tissue injury in response to heat stress and cooling treatment in mice.

@article{Liu2011IntestinalIA,
  title={Intestinal inflammation and tissue injury in response to heat stress and cooling treatment in mice.},
  author={Zhifeng Liu and Xuegang Sun and Jing Tang and You-qing Tang and Huasheng Tong and Qiang Wen and Yun-song Liu and Lei Su},
  journal={Molecular medicine reports},
  year={2011},
  volume={4 3},
  pages={
          437-43
        }
}
Gut-derived endotoxin and pathogenic bacteria have been proposed to be important causative factors of morbidity and mortality due to heat stroke. However, the molecular mechanisms underlying the small intestinal lesions caused by heat stroke have yet to be well characterized. In order to verify the possible inflammatory pathogenesis of intestinal tissue injury, a mouse heat stroke model was established. Cooling treatment was applied, mimicking the clinical therapy. Morphologic changes in… 
View on PubMed
spandidos-publications.com
40 Citations
Highly Influential Citations
2
Background Citations
17
Methods Citations
4
Results Citations
4

40 Citations

Citation Type

Citation Type

Cryptdin-2 predicts intestinal injury during heatstroke in mice
TLDR
It was found that HS upregulated the expression of Cry-2, and the serum and intestinal concentrations ofCry-2 were correlated with the severity of HS-induced intestinal damage, indicated by pathology scores and concentrations of DAO and D-lac.
Abstract. Intestinal injury-induced bacterial translocation and endotoxemia are important in the pathophysiological process of heatstroke. However, the underlying mechanism remains to be fully elucidated. Previous studies using 2D-gel electrophoresis found that defensin-related cryptdin-2 (Cry-2), a
  • 2017
Heat stress induces intestinal injury through lysosome- and mitochondria-dependent pathway in vivo and in vitro
TLDR
In these models, heat stress-induced apoptosis of small intestinal tissue and epithelial cells through accumulation of ROS and activation of the lysosomal–mitochondrial apoptotic pathway involved the release of cathepsin B.
Effects of propofol on damage of rat intestinal epithelial cells induced by heat stress and lipopolysaccharides
  • J. Tang, Y. Jiang, +4 authors Z. Liu
  • Medicine
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • 2013
TLDR
A model that can mimic the intestinal heat stress environment is developed and demonstrates the effects on intestinal epithelial cell damage, and indicated that propofol could be used as a therapeutic drug for the treatment of heat-stress-induced intestinal injuries.
Blockage of protease‐activated receptor 1 ameliorates heat‐stress induced intestinal high permeability and bacterial translocation
TLDR
It is demonstrated that PAR1 signaling pathway may play an important role in the heat stress‐induced elevation of intestinal permeability, bacterial translocation and the occurrence of endotoxemia.
Preventing necroptosis by scavenging ROS production alleviates heat stress-induced intestinal injury
  • Li Li, Hongping Tan, +7 authors Z. Gu
  • Biology
    International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • 2020
TLDR
There is strong evidence that HS causes damage to both the small intestine and intestinal epithelial cells, and scavenging ROS production can significantly alleviate such RIPK1/RIPK3-dependent necroptosis, mediating HS-induced intestinal damage both in vitro and in vivo.
Intestinal Injury in Heat Stroke.
4-Phenylbutyrate Prevents Endoplasmic Reticulum Stress-Mediated Apoptosis Induced by Heatstroke in the Intestines of Mice
TLDR
Evidence that the beneficial effect of 4-PBA is closely related to the inhibition of ER stress-mediated apoptosis is provided, suggesting that ER stress may be a novel therapeutic target in patients with heatstroke.
Theanine supplementation prevents liver injury and heat shock response by normalizing hypothalamic-pituitaryadrenal axis hyperactivity in mice subjected to whole body heat stress
Regulatory T Cells Could Improve Intestinal Barrier Dysfunction in Heatstroke
TLDR
It is demonstrated that Tregs could improve HS-induced intestinal barrier dysfunction, probably via modulation of neutrophils in the intestine of mice during HS.
...
1
2
3
4
...

References

SHOWING 1-10 OF 31 REFERENCES
Inflammatory, hemostatic, and clinical changes in a baboon experimental model for heatstroke.
TLDR
The baboon model of heatstroke appears suitable for testing whether immunomodulation of the host's responses can improve outcome, and nonsurvivors displayed significantly greater coagulopathy, inflammatory activity, and tissue injury than survivors.
Time course of cytokine, corticosterone, and tissue injury responses in mice during heat strain recovery.
TLDR
The data suggest that the cytokine milieu changes during heat strain recovery with similarities between findings in mice and those described for human heatstroke, supporting the application of the model to the study of cytokine responses in vivo.
Selected contribution: Hyperthermia-induced intestinal permeability and the role of oxidative and nitrosative stress.
TLDR
Hyperthermia produced increased permeability and marked intestinal epithelial damage both in vivo and in vitro, suggesting that thermal disruption of epithelial membranes contributes to the intestinal barrier dysfunction manifested with heat stress.
Elevated pyrogenic cytokines in heatstroke.
TLDR
The findings of elevated circulating IL-6, IL-1 beta, and INF-gamma in the presence of acute phase response, and correlation with severity of illness, suggest that these cytokines have a role in the pathogenesis of heatstroke, which could lead to new therapeutic strategies.
Time course of endotoxemia and cardiovascular changes in heat-stressed primates.
TLDR
Endotoxemia may have been a contributing factor in the pathogenesis of heat stroke, and the use of anti-LPS antibodies may be expected to be beneficial.
Hypothermia in systemic inflammation: role of cytokines.
  • L. Leon
  • Biology
    Frontiers in bioscience : a journal and virtual library
  • 2004
TLDR
Suggested areas for future research include a determination of the final mediator of hypothermia and its specific anatomical site of action as well as the role of cytokines in the regulation of Hypothermia under non-inflammatory conditions.
Mechanisms of circulatory and intestinal barrier dysfunction during whole body hyperthermia.
TLDR
It is concluded that hyperthermia stimulates xanthine oxidase production of reactive oxygen species that activate metals and limit heat tolerance by promoting circulatory and intestinal barrier dysfunction and intact NOS activity is required for normal stress tolerance, whereas overproduction ofNO may contribute to the nonprogrammed splanchnic dilation that precedes vascular collapse with heat stroke.
The Roles of Exercise-Induced Immune System Disturbances in the Pathology of Heat Stroke
TLDR
The current evidence that supports the argument that exercise-induced immune and GI disturbances may contribute to the development of endotoxaemia and heat stroke is discussed.
HEAT SHOCK STRESS AMELIORATES CYTOKINE MIXTURE-INDUCED PERMEABILITY BY DOWNREGULATING THE NITRIC OXIDE AND SIGNAL TRANSDUCER AND ACTIVATOR OF TRANSCRIPTION PATHWAYS IN CACO-2 CELLS
TLDR
Cytomix increased epithelial permeability, which is associated with increased NO and STAT activities, possibly through the downregulation of the NO and Janus kinase/signal transducer and activator of transcription pathways.
Interleukin-6 induces thermotolerance in cultured Caco-2 cells independent of the heat shock response.
...
1
2
3
4
...