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

Inhibitors of Viral Protein Synthesis

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...

Inflammatory Response

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...

The Blood-brain Barrier

The Blood-brain Barrier

Inflammatory Response I: Vascular and Cellular

Inflammatory Response I: Vascular and Cellular

The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...

You might also read

Related Articles

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

Sort by

Same author

Endozoicomonas acroporae enhances coral thermal resilience through host-microbe coordination.

The ISME journal·2026

Same author

Niemann-Pick C1-Like 1 in Cholesterol Absorption and Homeostasis: Mechanisms, Regulation, and Emerging Phytochemical Inhibitors.

Current issues in molecular biology·2026

Same author

Microglial Nrf2 Functions as a Cell-Autonomous Regulator of Neuroinflammation and Trained Immunity in the Aging Brain.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology·2025

Same author

Jaceosidin, a natural polymethoxyflavone, suppresses leukemia cell growth and impairs lipid metabolism-dependent survival in AML and cytarabine-resistant cells.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2025

Same author

Endothelial type I interferon signaling modulates the vascular response to ischemic brain injury.

bioRxiv : the preprint server for biology·2025

Same author

Therapeutic peptides and their delivery using lipid-based nanoparticles.

Tzu chi medical journal·2025

Search research articles

Related Experiment Video

Updated: Mar 27, 2026

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Interferon-β Modulates Inflammatory Response in Cerebral Ischemia.

Ping-Chang Kuo¹, Barbara A Scofield¹, I-Chen Yu²

¹Department of Microbiology and Immunology, Indiana University School of Medicine, Fort Wayne, IN (P.C.K., B.A.S., J.H.Y.).

Journal of the American Heart Association

|January 10, 2016

Summary

Interferon-beta (IFNβ) reduces brain damage and neurological deficits in ischemic stroke models. This cytokine

Keywords:

CD4+ T cells Interferon‐β ischemic stroke microglia monocytes/macrophages neuroinflammation reperfusion γδ T cells

More Related Videos

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Published on: February 12, 2016

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Published on: July 5, 2024

Related Experiment Videos

Last Updated: Mar 27, 2026

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Published on: February 12, 2016

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Published on: July 5, 2024

Area of Science:

Neuroscience
Immunology
Pharmacology

Background:

Stroke is a leading global cause of death, often resulting from acute ischemic injury.
Interferon-beta (IFNβ), an approved immunomodulatory cytokine, possesses anti-inflammatory properties and a known safety profile.
IFNβ's characteristics suggest potential therapeutic value for treating ischemic stroke.

Purpose of the Study:

To investigate the therapeutic efficacy of Interferon-beta (IFNβ) in a mouse model of ischemic stroke.
To elucidate the molecular mechanisms underlying IFNβ's effects on ischemic brain inflammation.

Main Methods:

Utilized a mouse model of transient middle cerebral artery occlusion/reperfusion to simulate ischemic stroke.
Administered IFNβ to assess its impact on infarct size and neurological deficits.
Analyzed molecular changes in the ischemic brain, including immune cell infiltration and inflammatory mediator production.

Main Results:

IFNβ significantly reduced infarct volume in the ischemic brain.
IFNβ treatment lessened neurological deficits in animals subjected to ischemic stroke.
IFNβ modulated neuroinflammation by reducing immune cell infiltration, inflammatory mediator production, adhesion molecule expression, and microglia activation.

Conclusions:

IFNβ demonstrates a protective effect against ischemic stroke, primarily through its anti-inflammatory actions.
IFNβ is a potential therapeutic agent for mitigating reperfusion injury following stroke treatment.
Further research into IFNβ as a stroke therapy is warranted.