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

Colonisation of Pathogens

Colonisation of Pathogens

Pathogen colonization of host tissues is a critical step in the development of infectious diseases. Various pathogenic microorganisms, including bacteria, fungi, viruses, and protozoa, have evolved complex strategies to attach to, invade, and persist within host environments. These mechanisms enable pathogens to establish infections, evade immune responses, and resist antimicrobial treatments.Attachment to Host CellsIn bacteria, colonization typically begins with adherence to host epithelial...

Gastritis II: Pathophysiology

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...

Determinants of Bacterial Pathogenicity and Virulence

Determinants of Bacterial Pathogenicity and Virulence

Pathogenic bacteria employ a variety of strategies to establish infections, including the secretion of extracellular enzymes that act as potent virulence factors. These enzymes facilitate bacterial colonization of host tissues and help evade immune surveillance. By targeting structural components of host tissues and interfering with immune mechanisms, these enzymes play a pivotal role in disease progression.Extracellular Enzymes Facilitating Tissue Invasion: Several bacterial pathogens secrete...

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...

Regulation of Bacterial Virulence

Regulation of Bacterial Virulence

Pathogenic bacteria employ a range of regulatory mechanisms to modulate the expression of virulence genes in response to environmental and host-derived signals. These mechanisms ensure that virulence factors are expressed only under favorable conditions, thereby optimizing infection and survival strategies.Mechanisms of Virulence RegulationKey regulatory strategies include:Two-Component Systems: These consist of a membrane-bound sensor kinase and a cytoplasmic response regulator. Environmental...

You might also read

Related Articles

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

Sort by

Same author

Readability and Linguistic Characteristics of Alzheimer's Disease and Related Dementias Prevention, Symptom, and Treatment Information from Generative Artificial Intelligence Chatbots.

Journal of gerontological nursing·2026

Same author

Evaluating the experiences of Vietnamese university students enrolled in a longitudinal research cohort: a journey mapping approach.

Frontiers in medicine·2026

Same author

Development and Optimization of CRISPR/Cas9-Assisted Recombineering in <i>Escherichia albertii</i>.

microPublication biology·2026

Same author

Oral Colon-Targeted Lipid Nanoparticles Enhance Upadacitinib Delivery and Efficacy in a Murine Model of Ulcerative Colitis.

International journal of molecular sciences·2026

Same author

Combining Token Classification With Large Language Model Revision for Age-Friendly 4M Entity Recognition From Nursing Home Text Messages: Development and Evaluation Study.

medRxiv : the preprint server for health sciences·2026

Same author

Characterizing nursing home care team communication via text messaging: A social network analysis.

International journal of medical informatics·2026

Search research articles

Related Experiment Video

Updated: Jun 22, 2026

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells

Published on: September 18, 2016

Pathogenic bacteria induce colonic PepT1 expression: an implication in host defense response.

Hang Thi Thu Nguyen¹, Guillaume Dalmasso, Kimberly R Powell

¹Department of Medicine, Emory University, Atlanta, Georgia 30322, USA. hnguye9@emory.edu

Gastroenterology

|June 25, 2009

Summary

Pathogenic bacteria induce the di/tripeptide transporter PepT1 in the colon. This transporter plays a key role in host defense by reducing bacterial colonization and intestinal inflammation.

More Related Videos

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4⁺ T Cells to Immunodeficient Mice

Published on: December 16, 2021

Colonization with Murine pks+ Escherichia coli under Non-Inflammatory Conditions

Colonization with Murine pks+ Escherichia coli under Non-Inflammatory Conditions

Published on: March 10, 2026

Related Experiment Videos

Last Updated: Jun 22, 2026

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells

Development of an Antigen-driven Colitis Model to Study Presentation of Antigens by Antigen Presenting Cells to T Cells

Published on: September 18, 2016

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4⁺ T Cells to Immunodeficient Mice

Published on: December 16, 2021

Colonization with Murine pks+ Escherichia coli under Non-Inflammatory Conditions

Colonization with Murine pks+ Escherichia coli under Non-Inflammatory Conditions

Published on: March 10, 2026

Area of Science:

Gastroenterology
Microbiology
Immunology

Background:

Colonic di/tripeptide transporter PepT1 expression is known under inflammation.
Factors inducing colonic PepT1 and mechanisms are largely unknown.

Purpose of the Study:

Investigate the effects of pathogenic bacteria on colonic PepT1 expression.
Determine the functional consequences of PepT1 induction by pathogens.

Main Methods:

Infection of human colonic cells (HT29-Cl.19A) with enteropathogenic Escherichia coli (EPEC).
Infection of wild-type and PepT1 transgenic mice and cultured colonic tissues with Citrobacter rodentium.

Main Results:

EPEC induced PepT1 expression and activity in colonic cells via lipid rafts, requiring Cdx2.
PepT1 expression reduced EPEC binding, NF-κB and MAPK activation, and IL-8 production.
Citrobacter rodentium induced colonic PepT1 in mice; PepT1 transgenic mice showed reduced bacterial colonization and inflammation.

Conclusions:

A molecular mechanism for colonic PepT1 regulation by pathogens was identified.
PepT1 has a novel role in host defense against intestinal pathogens.
PepT1 modulates bacterial-epithelial interactions and reduces intestinal inflammation.