Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Role 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...

Inflammatory Response

Inflammatory 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,...

T Cell Types and Functions

T 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...

Mucosal Barrier of the Stomach

Mucosal 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...

Inflammatory Bowel Disease II: Ulcerative Colitis

Inflammatory 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...

Inflammatory Bowel Disease III: Crohn's Disease

Inflammatory 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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Gender and gut microbiota composition determine hepatic bile acid, metabolic and inflammatory response to a single fast-food meal in healthy adults.

Clinical nutrition (Edinburgh, Scotland)·2021

Same author

Long-term outcome of patients with advanced pancreatic cancer treated with sequential chemotherapies before the era of modern combination therapy protocols.

Journal of cancer research and clinical oncology·2018

Same author

Effects of the Mammalian Target of Rapamycin Inhibitor Everolimus on Hepatitis C Virus Replication In Vitro and In Vivo.

Transplantation proceedings·2017

Same author

Microarrays-Enabled Hypothesis Generation: The Suspect Role of FNBP-1 in Neuropsychiatric Pathogenesis Associated with HIV and/or HCV Infection.

Journal of AIDS & clinical research·2017

Same author

[Obeticholic acid in primary biliary cholangitis : PBC OCA international study of efficacy (POISE)].

Der Internist·2017

Same author

[Hepatology 2017: from basics to clinics - future perspectives].

Zeitschrift fur Gastroenterologie·2016

Search research articles

Related Experiment Video

Updated: May 11, 2026

Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine

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.

More Related Videos

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4⁺CD45RB^high T Cells into Immunodeficient Mice

Published on: April 21, 2015

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Published on: September 12, 2025

Related Experiment Videos

Last Updated: May 11, 2026

Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine

Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine

Published on: May 21, 2012

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4⁺CD45RB^high T Cells into Immunodeficient Mice

Published on: April 21, 2015

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Published on: September 12, 2025

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.