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

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...

Chronic Pancreatitis II: Pathophysiology

Chronic Pancreatitis II: Pathophysiology

Chronic pancreatitis is a progressive and irreversible inflammation of the pancreas, most often caused by long-term alcohol abuse, but it can also be related to ductal obstruction, smoking, or genetic factors.Chronic pancreatitis occurs when the pancreas is repeatedly exposed to harmful agents like alcohol, smoking, ductal obstruction, or genetic predisposition. These factors lead to the release of toxic metabolites and inflammatory cytokines, sustaining chronic inflammation in the pancreatic...

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...

Drugs for Treatment of Ulcerative Colitis in IBD

Drugs for Treatment of Ulcerative Colitis in IBD

Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide generation.

Chronic Pancreatitis I: Introduction

Chronic Pancreatitis I: Introduction

The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...

You might also read

Related Articles

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

Sort by

Same author

Different connectivity patterns of MRI-negative drug-resistant epilepsy and drug-sensitive epilepsy in cerebellar and subcortical-cortical regions.

Neurobiology of disease·2026

Same author

Aftiphilin Regulation of Myosin Light Chain Kinase Activity Promotes Actin Dynamics and Intestinal Epithelial Barrier Function.

Frontiers in gastroenterology (Lausanne, Switzerland)·2026

Same author

A human case of Q fever associated with cat in China: a neglected risk factor of Q fever.

One health outlook·2026

Same author

Mucosally sourced complement factor B modulates the host response to colitis.

bioRxiv : the preprint server for biology·2026

Same author

FSEA: Incorporating domain-specific prior knowledge for few-shot weed detection.

Plant phenomics (Washington, D.C.)·2025

Same author

Integrated genomic and transcriptomic profiling of glioblastoma reveals ecDNA-driven heterogeneity and microenvironmental reprogramming.

Cell reports·2025

Search research articles

Related Experiment Video

Updated: Jun 8, 2026

Chronic Salmonella Infection Induced Intestinal Fibrosis

Chronic Salmonella Infection Induced Intestinal Fibrosis

Published on: September 22, 2019

Substance P modulates colitis-associated fibrosis.

Hon Wai Koon¹, David Shih, Iordanes Karagiannides

¹Inflammatory Bowel Disease Center, Division of Digestive Diseases, David Geffen School of Medicine, University of California, Los Angeles, MRL Building, Room 1240, 675 Charles E. Young Dr. South, Los Angeles, CA 90095, USA.

The American Journal of Pathology

|October 5, 2010

Summary

Substance P (SP) and its receptor (NK-1R) drive intestinal fibrosis in chronic colitis. Blocking NK-1R or its absence reduces fibrosis by inhibiting fibroblast activation and collagen production.

More Related Videos

Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue

Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue

Published on: October 12, 2013

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease

Published on: March 1, 2022

Related Experiment Videos

Last Updated: Jun 8, 2026

Chronic Salmonella Infection Induced Intestinal Fibrosis

Chronic Salmonella Infection Induced Intestinal Fibrosis

Published on: September 22, 2019

Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue

Isolation of Primary Myofibroblasts from Mouse and Human Colon Tissue

Published on: October 12, 2013

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease

A TNBS-Induced Rodent Model to Study the Pathogenic Role of Mechanical Stress in Crohn's Disease

Published on: March 1, 2022

Area of Science:

Gastroenterology
Immunology
Fibrosis Research

Background:

Substance P (SP) and neurokinin-1 receptor (NK-1R) signaling are implicated in colitis and mucosal healing.
Colonic fibrosis is a significant complication of chronic inflammatory bowel diseases.

Purpose of the Study:

To investigate the role of SP and NK-1R in the development of colonic fibrosis during chronic colitis.
To determine if SP modulates fibrotic processes via NK-1R in a mouse model of colitis.

Main Methods:

Utilized a chronic trinitrobenzenesulfonic acid (TNBS)-induced colitis model in wild-type (WT) and NK-1R knockout (NK-1R KD) mice.
Assessed colonic fibrosis through mRNA expression of collagen and fibrogenic factors, and immunohistochemical collagen deposition.
Administered an NK-1R antagonist (CJ-12255) to TNBS-exposed WT mice.
Examined SP-induced effects on human colonic fibroblasts (CCD-18Co) in vitro.

Main Results:

Chronic TNBS colitis increased collagen, vimentin, TGF-β1, and IGF-1 expression in WT mice, indicating fibrosis.
NK-1R antagonist treatment and NK-1R deficiency significantly reduced colonic fibrosis, inflammation, and fibrogenic factor expression.
NK-1R was co-localized with fibroblasts in inflamed colons and human Crohn's disease mucosa.
SP exposure enhanced fibroblast migration and collagen synthesis in vitro, an effect mediated by TGF-β1 and IGF-1.

Conclusions:

SP, acting through NK-1R, promotes intestinal fibrogenesis in chronic colitis.
Targeting the SP/NK-1R pathway may offer a therapeutic strategy to mitigate colonic fibrosis in inflammatory bowel diseases.