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Related Experiment Videos

Thermal stress induces epithelial permeability

P L Moseley1, C Gapen, E S Wallen

  • 1Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.

The American Journal of Physiology
|August 1, 1994
PubMed
Summary

Elevated temperatures increase gut epithelial permeability, potentially causing organ failure. Prior heat stress, inducing heat-shock protein 70 (HSP 70), raises the temperature threshold required to disrupt this barrier, offering cellular protection.

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Area of Science:

  • Physiology
  • Cell Biology
  • Biophysics

Background:

  • Heat injury can lead to multiorgan system failure, with gut epithelial permeability changes suspected as a key factor.
  • Endotoxemia and intestinal hemorrhage in heat injury suggest compromised gut barrier function.

Purpose of the Study:

  • To investigate heat-induced alterations in epithelial barrier integrity at physiologically relevant temperatures.
  • To determine if prior heat stress influences the response of epithelial cells to subsequent thermal challenges.

Main Methods:

  • Utilized a high-resistance Madin-Darby canine kidney epithelial cell clone to model gut epithelium.
  • Measured transepithelial electrical conductance and mannitol permeability across cell monolayers at varying temperatures.
  • Applied a conditioning heat stress (42°C for 90 min) and assessed subsequent thermal responses and cell survival.

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Main Results:

  • Heating epithelial cell monolayers above 38.3°C increased transepithelial electrical conductance and mannitol permeability, indicating increased paracellular permeability.
  • A conditioning heat stress 48 hours prior shifted the temperature threshold for conductance increase to 39.4°C and conferred thermotolerance.
  • Heat-shock protein 70 (HSP 70) accumulated 48 hours after conditioning heat stress but returned to baseline by 96 hours.

Conclusions:

  • Mild temperature elevations can disrupt epithelial barrier integrity by increasing paracellular permeability.
  • Preconditioning heat stress, associated with HSP 70 induction, enhances epithelial thermotolerance by raising the disruption threshold.
  • These findings highlight the role of epithelial barrier function and heat-shock proteins in the response to thermal injury.