Related Experiment Video
Updated: May 11, 2026
09:25
Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
Published on: May 21, 2012
Toll-like receptor 2 controls mucosal inflammation by regulating epithelial barrier function
E Cario1, G Gerken, D K Podolsky
1Division of Gastroenterology & Hepatology, University Hospital of Essen and Medical School/University of Duisburg-Essen, Essen, Germany. elke.cario@uni-due.de
Gastroenterology
|April 6, 2007
Summary
Toll-like receptor 2 (TLR2) activation preserves intestinal barrier integrity by promoting cell survival and reducing inflammation. This suggests TLR2 is a potential therapeutic target for modulating mucosal injury and gut inflammation.
Area of Science:
- Immunology
- Gastroenterology
- Cell Biology
Background:
- Toll-like receptors (TLRs) are crucial for innate immunity and microbial recognition.
- Commensal bacteria maintain intestinal epithelial barrier stability, but mechanisms are unclear.
- Understanding TLR2's role in intestinal barrier integrity is vital for mucosal homeostasis.
Purpose of the Study:
- To investigate the functional role of TLR2 in maintaining tight junction (TJ)-associated intestinal epithelial barrier integrity.
- To elucidate how TLR2 balances mucosal homeostasis against inflammatory stress.
Main Methods:
- Utilized in vitro and ex vivo models of intestinal epithelial cells (IECs) with TLR2 ligand stimulation.
- Assessed TJ-associated barrier assembly using Western blotting and confocal microscopy.
- Investigated DSS colitis in wild-type, TLR2-/-, and MyD88-/- mice, assessing apoptosis and TJ disruption.
Main Results:
- TLR2 stimulation preserved TJ integrity against stress via PI3K/Akt-mediated survival through MyD88.
- TLR2 deficiency led to early TJ disruption and apoptosis during inflammatory stress in mice.
- Oral TLR2 ligand (PCSK) treatment suppressed colitis by restoring TJ integrity and reducing apoptosis.
Conclusions:
- TLR2 plays a critical role in regulating intestinal epithelial barrier integrity.
- TLR2 activation protects against inflammatory stress-induced mucosal injury.
- TLR2 represents a potential therapeutic target for managing intestinal inflammation and injury.
Related Concept Videos
01:12Role Of Notch Signalling In Intestinal Stem Cell Renewal
Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
01:28Inflammatory Response
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
01:24T Cell Types and Functions
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
01:25Mucosal Barrier of the Stomach
The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
01:20Inflammatory Bowel Disease II: Ulcerative Colitis
Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
01:25Inflammatory Bowel Disease III: Crohn's Disease
Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...