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

Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

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...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
Inflammation01:38

Inflammation

Overview
Inflammatory Response01:28

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,...
Inflammatory Response I: Vascular and Cellular01:30

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,...
Inflammation: Introduction01:28

Inflammation: Introduction

Inflammation is a fundamental, protective biological response of vascularized tissues to cellular injury, infection, or harmful stimuli. Its primary function is to eliminate the initial cause of injury, clear necrotic cells and damaged tissue, and initiate the necessary repair processes.Cardinal SignsAcute inflammation presents with classic signs. Redness results from vasodilation and increased blood flow. Heat is due to increased metabolism and circulation. Swelling results from the...

You might also read

Related Articles

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

Sort by
Same author

Platelet-leucocyte interactions drive MMP-mediated tissue damage in tuberculosis.

PLoS pathogens·2026
Same author

Towards host-directed therapy: The role of matrix metalloproteinases in the immunopathogenesis of tuberculosis.

International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases·2026
Same author

Viral infections and invasive group a streptococcal disease incidence during 2022-2023.

The Lancet regional health. Europe·2026
Same author

Neutrophils in idiopathic pulmonary fibrosis patients are phenotypically distinct from controls.

ERJ open research·2025
Same author

Mortality Among Patients With Invasive Group A Streptococcal Infections Caused by the M1UK Lineage: A Retrospective Cohort Study in England and Wales.

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America·2025
Same author

Immunity to Streptococcus pyogenes and Common Respiratory Viruses at Age 0 to 4 Years After COVID-19 Restrictions.

JAMA network open·2025
Same journal

Future perspectives on regulating pro-and anti-inflammatory responses in sepsis.

Contributions to microbiology·2011
Same journal

Regulation of pro-and anti-inflammatory host responses.

Contributions to microbiology·2011
Same journal

Anti-inflammatory mechanisms of sepsis.

Contributions to microbiology·2011
Same journal

Molecular mechanisms of sepsis.

Contributions to microbiology·2011
Same journal

Virulence factors of gram-negative bacteria in sepsis with a focus on Neisseria meningitidis.

Contributions to microbiology·2011
Same journal

Clinical aspects of sepsis.

Contributions to microbiology·2011
See all related articles

Related Experiment Video

Updated: Jun 1, 2026

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats
05:56

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

Published on: February 20, 2021

Pro-inflammatory mechanisms in sepsis.

Deborah L W Chong, Shiranee Sriskandan

    Contributions to Microbiology
    |June 11, 2011
    PubMed
    Summary
    This summary is machine-generated.

    Sepsis involves a severe inflammatory response to infection. This review details how the body recognizes pathogens via pattern recognition receptors (PRRs) and triggers inflammation, leading to a

    More Related Videos

    A Data-Driven Approach to Quantifying Immune States in Sepsis
    07:42

    A Data-Driven Approach to Quantifying Immune States in Sepsis

    Published on: February 7, 2025

    Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation
    07:48

    Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation

    Published on: May 16, 2016

    Related Experiment Videos

    Last Updated: Jun 1, 2026

    A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats
    05:56

    A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

    Published on: February 20, 2021

    A Data-Driven Approach to Quantifying Immune States in Sepsis
    07:42

    A Data-Driven Approach to Quantifying Immune States in Sepsis

    Published on: February 7, 2025

    Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation
    07:48

    Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation

    Published on: May 16, 2016

    Area of Science:

    • Immunology
    • Pathology
    • Microbiology

    Background:

    • Sepsis is a life-threatening condition characterized by a dysregulated hyper-inflammatory host response to microbial infection.
    • Pathogen recognition by host immune cells is a critical initial step in initiating the inflammatory cascade.
    • Understanding these host mechanisms is crucial for developing effective sepsis treatments.

    Purpose of the Study:

    • To review current knowledge on host mechanisms mediating the hyper-inflammatory response in sepsis.
    • To synthesize information on pathogen recognition pathways and subsequent pro-inflammatory signaling.
    • To elucidate the roles of various mediators in sepsis-induced inflammation.

    Main Methods:

    • Literature review of current research on sepsis pathogenesis.
    • Analysis of host pattern recognition receptors (PRRs) and their signaling pathways.
    • Examination of inflammatory mediators and their involvement in vascular and cellular responses.

    Main Results:

    • Pattern recognition receptors (PRRs), including Toll-like, C-type lectin, RIG-1-like, and Nod-like receptors, are key in initiating sepsis inflammation.
    • Nod-like receptors are involved in inflammasome formation, crucial for pro-inflammatory cytokine maturation.
    • Bacterial superantigens exploit host receptors to induce a 'cytokine storm', amplifying the inflammatory response.

    Conclusions:

    • Host recognition of microbial ligands via PRRs is central to sepsis-induced inflammation.
    • The inflammatory response involves complex interactions between microbial products, host receptors, and alarmins.
    • Key mediators orchestrate vascular changes, endothelial permeability, coagulation, and leukocyte activation in sepsis.