In Vivo Mouse Intestinal Permeability Study
Objective: Assessment of LPS-induced increases in mouse intestinal permeability and associated protein activation in vivo, investigating the TLR-4/FAK/MyD88 signal transduction pathway
This is a In Vivo Mouse Intestinal Permeability Study protocol using mouse as the model organism. The procedure involves 3 procedural steps, 1 materials. Extracted from a 2015 paper published in The Journal of Immunology.
Model and subjects
mouse • Not specified in provided text • unknown • Not specified in provided text • Not specified in provided text
Study window
Estimated timing pending
Core workflow
In vivo LPS administration and intestinal permeability assessment • Assessment of intestinal epithelial FAK knockdown effects • Assessment of high-dose LPS-induced intestinal inflammation
Primary readouts
- Intestinal tight junction permeability (TJP) changes
- FAK activation and localization
- MyD88 activation
- IRAK4 activation
Key equipment and reagents
Verified items
0
Direct vendor links
0
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Protocol Steps
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In vivo LPS administration and intestinal permeability assessment
LPS was administered to mice in vivo to induce intestinal permeability changes. The study assessed LPS-induced increase in mouse intestinal permeability and associated protein activation.
Note: In vivo studies confirmed that LPS-induced increase in mouse intestinal permeability was associated with FAK and MyD88 activation
View evidence from paper
“In-vivo studies also confirmed that LPS-induced increase in mouse intestinal permeability was associated with FAK and MyD88 activation”
Assessment of intestinal epithelial FAK knockdown effects
Knockdown of intestinal epithelial FAK was performed to determine its role in LPS-induced intestinal permeability changes.
Note: FAK knockdown prevented LPS-induced increase in intestinal permeability
View evidence from paper
“knockdown of intestinal epithelial FAK prevented LPS-induced increase in intestinal permeability”
Assessment of high-dose LPS-induced intestinal inflammation
High dose LPS was administered to assess intestinal inflammation and its dependence on the TLR-4/FAK/MyD88 signaling axis.
Note: High dose LPS-induced intestinal inflammation was dependent on TLR-4/FAK/MyD88 signal-transduction axis
View evidence from paper
“high dose LPS-induced intestinal inflammation was also dependent on TLR-4/FAK/MyD88 signal-transduction axis”