Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Inflammatory Bowel Disease III: Crohn's Disease01:25

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...
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

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 Response01:28

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,...
Inflammatory Bowel Disease IV: Pharmacological Management01:29

Inflammatory Bowel Disease IV: Pharmacological Management

Upon diagnosis, managing Inflammatory Bowel Disease (IBD) involves addressing several crucial aspects. The primary goals include resting the bowel, correcting malnutrition, and providing symptomatic relief. Resting the bowel may consist of medications to reduce inflammation and promote healing. Correcting malnutrition is essential, often requiring dietary adjustments and nutritional supplements. Symptomatic relief aims to ease pain, diarrhea, and other discomforts in IBD.
Pharmacologic...
Dysbiosis of the Gut Microbiota01:18

Dysbiosis of the Gut Microbiota

The human gut microbiome includes a diverse array of microbial species, including beneficial commensals and opportunistic pathogens, which interact to support host health. These microbes contribute to essential functions such as nutrient metabolism, immune system modulation, and maintenance of intestinal barrier integrity. However, disruptions to this equilibrium—referred to as dysbiosis—can have widespread physiological consequences.Dysbiosis is often characterized by reduced microbial...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...

You might also read

Related Articles

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

Sort by
Same author

Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB<sub>1</sub>, TRPV1, and PPARα.

Biochemical pharmacology·2019
Same author

A systematic review of cannabidiol dosing in clinical populations.

British journal of clinical pharmacology·2019
Same author

Liver retraction techniques for laparoscopic cholecystectomy.

Surgical endoscopy·2017
Same author

The endogenous cannabinoid anandamide increases human airway epithelial cell permeability through an arachidonic acid metabolite.

Pharmacological research·2016
Same author

Students in medical school become involved in research for many reasons.

Irish medical journal·2013
Same author

Studies in Neotropical Paleobotany. XV. A Mio-Pliocene palynoflora from the Eastern Cordillera, Bolivia: implications for the uplift history of the Central Andes.

American journal of botany·2011

Related Experiment Video

Updated: May 31, 2026

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
07:32

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance

Published on: December 3, 2020

Cannabinoids mediate opposing effects on inflammation-induced intestinal permeability.

A Alhamoruni1, K L Wright, M Larvin

  • 1School of Graduate Entry Medicine & Health, Derby City General Hospital, University of Nottingham, Derby, UK.

British Journal of Pharmacology
|July 13, 2011
PubMed
Summary

Phytocannabinoids like THC and CBD can reverse inflammation-induced intestinal permeability changes by acting on CB(1) receptors. Endocannabinoids play a role in mediating these inflammatory effects.

More Related Videos

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
09:04

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Published on: February 27, 2014

Systematic Scoring Analysis for Intestinal Inflammation in a Murine Dextran Sodium Sulfate-Induced Colitis Model
09:11

Systematic Scoring Analysis for Intestinal Inflammation in a Murine Dextran Sodium Sulfate-Induced Colitis Model

Published on: February 14, 2021

Related Experiment Videos

Last Updated: May 31, 2026

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
07:32

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance

Published on: December 3, 2020

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
09:04

DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat

Published on: February 27, 2014

Systematic Scoring Analysis for Intestinal Inflammation in a Murine Dextran Sodium Sulfate-Induced Colitis Model
09:11

Systematic Scoring Analysis for Intestinal Inflammation in a Murine Dextran Sodium Sulfate-Induced Colitis Model

Published on: February 14, 2021

Area of Science:

  • Gastroenterology
  • Pharmacology
  • Cell Biology

Background:

  • Cannabinoid receptor activation influences emesis, inflammation, and gastric acid secretion.
  • Modulating intestinal permeability during inflammation is crucial for maintaining epithelial barrier integrity.
  • The role of cannabinoids in regulating inflammation-induced intestinal permeability requires further investigation.

Purpose of the Study:

  • To investigate whether cannabinoids can modulate the increased intestinal permeability associated with inflammation in vitro.
  • To explore the potential therapeutic applications of cannabinoids in managing inflammatory conditions affecting the gut.

Main Methods:

  • Caco-2 cell monolayers were inflamed using IFNγ and TNFα.
  • Transepithelial electrical resistance and flux measurements assessed monolayer permeability.
  • Cannabinoids and receptor antagonists (CB(1), CB(2), TRPV1, PPARγ, PPARα) were used to determine mechanisms of action.

Main Results:

  • Δ(9)-Tetrahydrocannabinol (THC) and cannabidiol accelerated recovery from cytokine-induced permeability increases, mediated by CB(1) receptors.
  • Endocannabinoids (anandamide, 2-arachidonylglycerol) exacerbated permeability, also via CB(1) receptors.
  • Inhibiting endocannabinoid breakdown worsened permeability, while inhibiting synthesis attenuated it.

Conclusions:

  • Locally produced endocannabinoids, acting via CB(1) receptors, mediate inflammation-related permeability changes.
  • Phytocannabinoids demonstrate therapeutic potential for reversing disordered intestinal permeability in inflammatory conditions.