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

Chronic Bowel Disorders: Introduction01:17

Chronic Bowel Disorders: Introduction

Chronic bowel diseases are a group of long-term conditions affecting the digestive tract, characterized by inflammation and damage to the gut lining. These conditions primarily include irritable bowel syndrome and inflammatory bowel disease.
Irritable Bowel Syndrome (IBS) is a common disorder affecting the gastrointestinal tract. The distinctive feature is recurrent abdominal pain associated with altered bowel movements, manifesting as constipation, diarrhea, or fluctuating between both. The...
Inflammatory Bowel Disease I: Ulcerative Colitis01:27

Inflammatory Bowel Disease I: Ulcerative Colitis

Introduction
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid receptor...
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 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...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...

You might also read

Related Articles

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

Sort by
Same author

Novel immunohistochemical assay utilizing the INSM1 (SP493) antibody demonstrates high specificity and sensitivity in detecting primary neuroendocrine lung neoplasms.

Diagnostic pathology·2025
Same author

Extracellular Nicotinamide Phosphoribosyltransferase Is a Therapeutic Target in Experimental Necrotizing Enterocolitis.

Biomedicines·2024
Same author

Global Frequency Analyses of Canine Progressive Rod-Cone Degeneration-Progressive Retinal Atrophy and Collie Eye Anomaly Using Commercial Genetic Testing Data.

Genes·2023
Same author

<i>Clostridium scindens</i> exacerbates experimental necrotizing enterocolitis via upregulation of the apical sodium-dependent bile acid transporter.

American journal of physiology. Gastrointestinal and liver physiology·2023
Same author

Enteral Feeding and Antibiotic Treatment Do Not Influence Increased Coefficient of Variation of Total Fecal Bile Acids in Necrotizing Enterocolitis.

Newborn (Clarksville, Md.)·2023
Same author

Investigation of a common canine factor VII deficiency variant in dogs with unexplained bleeding on autopsy.

Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc·2022

Related Experiment Video

Updated: May 8, 2026

Ileectomy-induced Bile Overaccumulation in Mouse Intestine
06:55

Ileectomy-induced Bile Overaccumulation in Mouse Intestine

Published on: August 21, 2017

Bile acids induce ileal damage during experimental necrotizing enterocolitis.

Melissa D Halpern1, Hana Holubec, Tara A Saunders

  • 1Department of Pediatrics, Steele Children's Research Center, University of Arizona, Tucson, 85724, USA. mhalpern@peds.arizona.edu

Gastroenterology
|February 14, 2006
PubMed
Summary

Bile acids (BAs) contribute to ileal damage in necrotizing enterocolitis (NEC), a common premature infant emergency. Reducing ileal BAs lessened NEC severity, suggesting a therapeutic target for this condition.

More Related Videos

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis
05:39

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

Published on: November 30, 2021

In Vitro Apical-Out Enteroid Model of Necrotizing Enterocolitis
09:11

In Vitro Apical-Out Enteroid Model of Necrotizing Enterocolitis

Published on: June 8, 2022

Related Experiment Videos

Last Updated: May 8, 2026

Ileectomy-induced Bile Overaccumulation in Mouse Intestine
06:55

Ileectomy-induced Bile Overaccumulation in Mouse Intestine

Published on: August 21, 2017

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis
05:39

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

Published on: November 30, 2021

In Vitro Apical-Out Enteroid Model of Necrotizing Enterocolitis
09:11

In Vitro Apical-Out Enteroid Model of Necrotizing Enterocolitis

Published on: June 8, 2022

Area of Science:

  • Gastroenterology
  • Neonatology
  • Pediatric Surgery

Background:

  • Necrotizing enterocolitis (NEC) is a critical gastrointestinal emergency in premature infants.
  • Bile acids (BAs) are known to cause intestinal mucosal injury.
  • The specific role of BAs in NEC development remains to be fully elucidated.

Purpose of the Study:

  • To investigate the contribution of bile acids (BAs) to the development of necrotizing enterocolitis (NEC) in a neonatal rat model.
  • To explore the impact of BA levels and transport mechanisms on NEC pathogenesis.

Main Methods:

  • Neonatal rats were induced with NEC using formula feeding, asphyxia, and cold stress.
  • Measurements included jejunal and ileal luminal BAs, portal blood BAs, and expression of BA transporters (ASBT, IBABP, Ostalpha/Ostbeta).

Main Results:

  • Ileal luminal BA levels significantly increased during NEC development.
  • Ileal BA removal decreased NEC incidence and severity.
  • Increased ileal BAs correlated with NEC severity, and treatment with epidermal growth factor (EGF) reduced both.

Conclusions:

  • Bile acids play a significant role in ileal damage during experimental NEC.
  • Altered bile acid transport in the neonatal ileum may contribute to NEC development.
  • Targeting bile acids presents a potential therapeutic strategy for NEC.