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Updated: Dec 13, 2025

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
Published on: December 3, 2020
Actin cytoskeleton dynamics during mucosal inflammation: a view from broken epithelial barriers
Susana Lechuga1, Andrei I Ivanov1
1Department of Inflammation and Immunity, Lerner Research Institute of Cleveland Clinic Foundation, Cleveland, OH 44195.
Epithelial barrier disruption during mucosal inflammation is driven by the actin cytoskeleton. This review details how cytoskeletal changes lead to leaky barriers and tissue damage.
Area of Science:
- Cell Biology
- Immunology
- Gastroenterology
Background:
- Epithelial barrier disruption is central to mucosal inflammation, triggering immune responses and tissue damage.
- Impaired epithelial barrier function stems from altered adherens and tight junctions due to inflammatory stimuli.
- The actin cytoskeleton plays a critical role in regulating epithelial junction integrity.
Purpose of the Study:
- To review the role of the actin cytoskeleton in epithelial junction disruption during mucosal inflammation.
- To summarize recent advances in understanding cytoskeletal remodeling in epithelial barrier homeostasis and disruption.
- To discuss the impact of the inflamed tissue microenvironment on the actomyosin cytoskeleton.
Main Methods:
- Literature review of recent advances in cell biology and immunology.
- Focus on the mechanisms of cytoskeletal remodeling, including actin filament dynamics and myosin II contractility.
- Analysis of how inflammatory environments affect the junction-associated actomyosin cytoskeleton.
Main Results:
- Actin cytoskeleton remodeling, through filament turnover and myosin II activity, is crucial for maintaining epithelial barrier function.
- During mucosal inflammation, cytoskeletal changes disrupt epithelial junctions, leading to increased permeability.
- The altered biochemical and physical properties of inflamed tissues influence actomyosin dynamics, exacerbating barrier disruption.
Conclusions:
- The actin cytoskeleton is a key mediator of epithelial barrier dysfunction in mucosal inflammation.
- Understanding cytoskeletal regulation offers potential therapeutic targets for inflammatory diseases.
- The interplay between the inflamed microenvironment and the actomyosin cytoskeleton is critical for barrier integrity.
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