Epithelial Injury
Epithelial Injury - Related Videos
06:23
Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
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2025
Here, we describe an in vitro protocol to model hypoxia/reoxygenation damage in the highly metabolic proximal tubular epithelial cells. This model is designed to induce metabolic stress-induced damage, which can be measured through the expression of proximal tubule damage markers and assessment of mitochondrial respiratory function.
07:28
Controlled Cervical Laceration Injury in Mice
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Cited by 17 •
2013
A novel technique to create a reproducible in vivo model of cervical spinal cord laceration injury in the mouse is described. This technique is based on spine stabilization by fixation of the cervical facets and laceration of the spinal cord using an oscillating blade with an accuracy of ±0.01 mm.
04:19
A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
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Cited by 16 •
2017
Athletes absorb several hundred mild traumatic brain injuries (mTBI)/concussions every year; however, the consequence of these on the brain is poorly understood. Therefore, an animal model of single and repetitive mTBI that consistently replicates clinically relevant symptoms provides the means to advance the study of mTBI and concussion.
08:51
Mammary Epithelial Transplant Procedure
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Cited by 23 •
2010
This article demonstrates the procedure developed by DeOme KB et al. (1959) and the sparing procedure developed by Brill B et al. (2008) for clearing the 4th inguinal mammary fat pad of a pubescent mouse in preparation for transplantation of mammary fragments, mammary epithelial cells, or mammary tumor cells.
10:09
Rapid Genetic Analysis of Epithelial-Mesenchymal Signaling During Hair Regeneration
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Cited by 10 •
2013
Tissue-specific analysis of a hair follicle regeneration model using lentivirus to mediate gain- or loss-of-function.
FAQs
Loss of cell junctions weakens the connections that maintain separation between epithelial cells, while membrane damage compromises the cells themselves. Together, these changes can increase access for pathogens and environmental threats and expose injured tissue to danger signals. The resulting barrier failure links local structural damage with activation of innate immune cells, cytokine production, and inflammation.
Danger signals provide an early indication that epithelial tissue has been damaged, even before the eventual outcome of infection or repair is established. Their release can activate innate immune cells and promote cytokine production, initiating inflammation. This response may help address an immediate threat, but the overview also links persistent inflammatory activity with progression toward chronic tissue damage.
Successful repair depends on coordinated epithelial cell migration and proliferation, followed by restoration of barrier function. Migration helps cover the damaged area, whereas proliferation supplies additional cells for rebuilding the layer. Repair is therefore not complete merely because tissue closes; the protective barrier must also be re-established to limit continued exposure to microbes and environmental threats.
Physical, chemical, and infectious insults represent distinct ways to initiate epithelial damage, although the overview identifies shared consequences. Each can disrupt cell junctions or membrane integrity, enabling pathogen entry and releasing danger signals. Comparing these insult types helps immunology and infection researchers separate the initiating cause from the common downstream processes of innate activation, cytokine production, inflammation, and repair.
These models provide a framework for examining how barrier failure initiates disease and changes host–pathogen interactions. Researchers can use them to consider pathogen entry, danger-signal release, innate immune activation, cytokine production, inflammation, and subsequent repair within one biological sequence. They also help relate early epithelial damage to later outcomes, including chronic tissue damage.
Studies can clarify how protective inflammation begins after barrier disruption and how that response changes as repair proceeds. They may also reveal why failure to restore epithelial integrity permits continued interaction between microbes and underlying tissue. This context is important for understanding the transition from an initially protective response to chronic tissue damage during infection-related disease.