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

Introduction to Fibroblasts

Introduction to Fibroblasts

Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation

Cystic Fibrosis: Pathogenesis

Cystic Fibrosis: Pathogenesis

Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation,...

Cystic Fibrosis: Management

Cystic Fibrosis: Management

Cystic fibrosis (CF) is an autosomal recessive disorder that predominantly affects individuals of Northern European descent, occurring at a rate of 1 in 3500. It is caused by a genetic mutation in a gene on chromosome 7, most commonly the ΔF508 mutation, that codes for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This results in thicker mucus secretions and obstruction pathologies in multiple organs, including the lungs and sinuses.
Sinus disease and chronic...

You might also read

Related Articles

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

Sort by

Same author

Author Correction: cBAF complex components and MYC cooperate early in CD8<sup>+</sup> T cell fate.

Nature·2026

Same author

Control of naive T cell reactivity and peripheral tolerance by ascorbate and TET activity.

Science advances·2026

Same author

A funnel approach to enable analyses of epitope-specific human CD4 T cells specific for influenza and SARS-CoV-2.

mBio·2026

Same author

Mice on a high-fat diet have reduced immunopathology and an altered immune response during respiratory syncytial virus infection.

mBio·2026

Same author

Efficient replication of influenza D virus in the human airway underscores zoonotic potential.

Proceedings of the National Academy of Sciences of the United States of America·2026

Same author

Rapid expansion of genotype D1.1 A(H5N1) influenza viruses in wild birds across North America during the 2024 migratory season.

Nature medicine·2026

Search research articles

Related Experiment Video

Updated: Dec 3, 2025

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

Exuberant fibroblast activity compromises lung function via ADAMTS4.

David F Boyd¹, E Kaitlynn Allen¹, Adrienne G Randolph^2,3

¹Department of Immunology, St Jude Children's Research Hospital, Memphis, TN, USA.

|October 29, 2020

Summary

This summary is machine-generated.

Severe respiratory infections can cause acute respiratory distress syndrome (ARDS). Targeting damage-responsive lung fibroblasts and their enzyme ADAMTS4 may improve outcomes for ARDS patients.

More Related Videos

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Published on: May 9, 2025

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis

Published on: December 21, 2014

Related Experiment Videos

Last Updated: Dec 3, 2025

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Refined Murine Model of Idiopathic Pulmonary Fibrosis

Published on: June 17, 2025

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Published on: May 9, 2025

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis

Implantation of Fibrin Gel on Mouse Lung to Study Lung-specific Angiogenesis

Published on: December 21, 2014

Area of Science:

Pulmonary Medicine
Immunology
Cell Biology

Background:

Severe respiratory infections can lead to acute respiratory distress syndrome (ARDS).
Current treatments for ARDS lack effective pharmacological therapies to improve patient outcomes.
While the host inflammatory response fights pathogens, immunopathology significantly contributes to tissue damage in ARDS.

Purpose of the Study:

To investigate the role of fibroblast activation states in respiratory viral infections and ARDS pathogenesis.
To identify specific fibroblast subsets and their contribution to lung immunopathology.
To explore potential therapeutic targets for mitigating ARDS severity.

Main Methods:

Characterization of fibroblast activation states induced by respiratory viral infection.
Analysis of extracellular matrix (ECM) remodeling enzymes, specifically ADAMTS4, produced by fibroblasts.
Correlation of ADAMTS4 levels in human subjects with influenza infection severity.

Main Results:

Respiratory viral infection induces distinct fibroblast states: ECM-synthesizing, damage-responsive, and interferon-responsive.
Excess activity of damage-responsive lung fibroblasts drives lethal immunopathology in severe influenza.
These fibroblasts produce ECM-remodelling enzymes like ADAMTS4 and inflammatory cytokines, promoting immune cell infiltration at the cost of lung function.
Elevated ADAMTS4 levels in the lower respiratory tract of human subjects correlated with influenza infection severity.

Conclusions:

Damage-responsive lung fibroblasts, through enzymes like ADAMTS4, significantly contribute to ARDS pathogenesis.
Targeting the ECM protease activity of these fibroblasts presents a potential therapeutic strategy.
Developing agents targeting damage-responsive fibroblasts could improve lung function and clinical outcomes in severe respiratory infections.