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

Myocarditis I: Introduction01:21

Myocarditis I: Introduction

645
Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
645
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

4.8K
Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...
4.8K
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

35
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...
35
T Cell Types and Functions01:24

T Cell Types and Functions

3.2K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
3.2K
Acute Inflammation II: Local and Systemic Effects01:25

Acute Inflammation II: Local and Systemic Effects

56
Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
56
Rheumatic Heart Disease I: Introduction01:23

Rheumatic Heart Disease I: Introduction

1.0K
Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
1.0K

You might also read

Related Articles

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

Sort by
Same author

Abnormal left ventricular subendocardial perfusion and diastolic function in women with obesity and heart failure and preserved ejection fraction.

The international journal of cardiovascular imaging·2023
Same author

QT Prolongation and In-Hospital Ventricular Arrhythmic Complications in Patients With Apical Ballooning Takotsubo Syndrome.

JACC. Clinical electrophysiology·2022
Same author

Contribution of hemoglobin concentration to cardiorespiratory fitness in black African American patients with recently decompensated heart failure and reduced ejection fraction.

Minerva cardiology and angiology·2022
Same author

Synergistic effect of myocardial injury and mid-regional proAdrenomedullin elevation in determining clinical outcomes of SARS-CoV-2 patients.

Frontiers in medicine·2022
Same author

Transition to rilonacept monotherapy from oral therapies in patients with recurrent pericarditis.

Heart (British Cardiac Society)·2022
Same author

Interleukin-1 and the NLRP3 inflammasome in COVID-19: Pathogenetic and therapeutic implications.

EBioMedicine·2022

Related Experiment Video

Updated: May 3, 2026

Isolation of Functional Cardiac Immune Cells
07:26

Isolation of Functional Cardiac Immune Cells

Published on: December 5, 2011

14.6K

Interleukin-18 mediates interleukin-1-induced cardiac dysfunction.

Stefano Toldo1, Eleonora Mezzaroma, Laura O'Brien

  • 1VCU Pauley Heart Center, Virginia Commonwealth University, Richmond, Virginia;

American Journal of Physiology. Heart and Circulatory Physiology
|February 18, 2014
PubMed
Summary

Interleukin-1 (IL-1) causes heart failure by releasing Interleukin-18 (IL-18), which impairs heart function. Blocking IL-18 may offer a targeted therapy for heart failure (HF).

Keywords:
heart failureinflammationinterleukinssystolic dysfunction

More Related Videos

Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1β using a Whole Blood Stimulation Assay
06:29

Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1β using a Whole Blood Stimulation Assay

Published on: March 1, 2011

25.4K
An IL-8 Transiently Transgenized Mouse Model for the In Vivo Long-term Monitoring of Inflammatory Responses
08:16

An IL-8 Transiently Transgenized Mouse Model for the In Vivo Long-term Monitoring of Inflammatory Responses

Published on: July 7, 2017

7.0K

Related Experiment Videos

Last Updated: May 3, 2026

Isolation of Functional Cardiac Immune Cells
07:26

Isolation of Functional Cardiac Immune Cells

Published on: December 5, 2011

14.6K
Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1β using a Whole Blood Stimulation Assay
06:29

Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1β using a Whole Blood Stimulation Assay

Published on: March 1, 2011

25.4K
An IL-8 Transiently Transgenized Mouse Model for the In Vivo Long-term Monitoring of Inflammatory Responses
08:16

An IL-8 Transiently Transgenized Mouse Model for the In Vivo Long-term Monitoring of Inflammatory Responses

Published on: July 7, 2017

7.0K

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Patients with heart failure (HF) exhibit elevated systemic IL-1 activity.
  • IL-1 is known to induce left ventricular (LV) systolic dysfunction in experimental models.
  • The precise mechanism by which IL-1 exerts these effects, specifically whether IL-18 is an intermediary, remains unclear.

Purpose of the Study:

  • To investigate whether IL-1-induced LV systolic dysfunction in mice is mediated by IL-18.
  • To evaluate the potential of IL-18 blockade as a therapeutic strategy for HF.

Main Methods:

  • Adult male mice were challenged with HF patient plasma or recombinant murine IL-1β.
  • Endogenous IL-18 was neutralized using recombinant human IL-18-binding protein (IL-18BP) or an IL-18-blocking antibody (IL-18AB).
  • LV fractional shortening, plasma IL-18, and IL-6 levels were measured. Genetic deletion models for IL-18 and its receptors were also utilized.

Main Results:

  • HF plasma and IL-1β induced LV systolic dysfunction, which was abrogated by IL-18AB or IL-18BP treatment.
  • IL-1β failed to induce LV systolic dysfunction in mice lacking IL-18 signaling.
  • While IL-1β increased plasma IL-18 and IL-6, IL-18 inhibition did not prevent IL-6 induction.

Conclusions:

  • IL-1 triggers the release of IL-18, which mediates LV systolic dysfunction in a mouse model of HF.
  • IL-18 does not appear to be the mediator for IL-1-induced IL-6 production.
  • Targeted blockade of IL-18 presents a promising therapeutic avenue for treating heart failure.