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...
Determinants of Bacterial Pathogenicity and Virulence01:20

Determinants of Bacterial Pathogenicity and Virulence

Pathogenic bacteria employ a variety of strategies to establish infections, including the secretion of extracellular enzymes that act as potent virulence factors. These enzymes facilitate bacterial colonization of host tissues and help evade immune surveillance. By targeting structural components of host tissues and interfering with immune mechanisms, these enzymes play a pivotal role in disease progression.Extracellular Enzymes Facilitating Tissue Invasion: Several bacterial pathogens secrete...
Gene Regulation in Microbial Communities: Quorum Sensing01:28

Gene Regulation in Microbial Communities: Quorum Sensing

Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
Cellular Injury I: Introduction01:00

Cellular Injury I: Introduction

Cellular injury occurs when a cell cannot maintain homeostasis or adapt to stressors such as hypoxia, toxins, or trauma. Depending on severity and duration, injury may be reversible, allowing recovery, or irreversible, leading to cell death.General Mechanisms of Cell InjuryAlthough causes vary, most cellular injuries arise from a few key mechanisms that disrupt essential functions and often amplify one another. Cell survival depends on the extent and balance of these disturbances.ATP depletion...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...

You might also read

Related Articles

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

Sort by
Same author

The Use of Kerecis Omega3 Wound Fish Skin Graft for the Treatment of Deep Burn Wounds.

Plastic and reconstructive surgery. Global open·2026
Same author

Safety and efficacy of bio-engineered, autologous dermo-epidermal skin grafts in reconstructive surgery: 1-year results of a prospective, randomized, intra-patient controlled, multicenter phase II clinical trial.

Journal of tissue engineering·2026
Same author

Extracellular Histones Associate with Blood-Brain Barrier Disruption and Astrocyte-Mediated Neuroinflammation During Polymicrobial Sepsis.

International journal of molecular sciences·2026
Same author

Remote Pancreatic Response to Severe Polytrauma Correlates With Clinical Outcome.

United European gastroenterology journal·2026
Same author

Safety and efficacy of bio-engineered, autologous dermo-epidermal skin grafts in adolescent and adult burn patients: 1-year results of a prospective, randomized, controlled, multicenter phase IIB clinical trial.

EClinicalMedicine·2025
Same author

Sarcoma Defect Reconstruction of the Posterior Trunk With Local Perforator Propeller Flaps.

ANZ journal of surgery·2025

Related Experiment Video

Updated: Jun 30, 2026

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
07:30

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

Harmful molecular mechanisms in sepsis.

Daniel Rittirsch1, Michael A Flierl, Peter A Ward

  • 1Department of Pathology, The University of Michigan Medical School, 1301 Catherine Road, Ann Arbor, Michigan 48109-0602, USA.

Nature Reviews. Immunology
|September 20, 2008
PubMed
Summary

Sepsis and multi-organ failure pose significant health challenges. This review explores the complex inflammatory network and immune response in sepsis, offering new insights into its pathophysiology.

Area of Science:

  • Immunology
  • Pathophysiology
  • Critical Care Medicine

Background:

  • Sepsis and associated multi-organ failure represent a major clinical and research challenge.
  • The complex pathophysiology of sepsis remains incompletely understood despite extensive investigation.
  • Sepsis is increasingly recognized as a dynamic and heterogeneous syndrome driven by inflammatory network imbalances.

Purpose of the Study:

  • To review recent advances in understanding sepsis pathophysiology.
  • To elucidate the molecular interactions during sepsis.
  • To unravel the nature of the dysregulated immune response in sepsis.

Main Methods:

  • Literature review of recent studies on sepsis.
  • Analysis of molecular interactions in sepsis.

More Related Videos

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis
05:28

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Published on: December 9, 2022

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

Related Experiment Videos

Last Updated: Jun 30, 2026

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
07:30

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis
05:28

Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis

Published on: December 9, 2022

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

  • Examination of immune response dysregulation in sepsis.
  • Main Results:

    • Sepsis is characterized by a complex and dynamic inflammatory network.
    • Molecular interactions reveal key pathways in sepsis development.
    • Immune response dysregulation is central to sepsis pathophysiology.

    Conclusions:

    • Understanding sepsis requires a focus on the inflammatory network and immune response.
    • Recent insights are improving our comprehension of sepsis heterogeneity.
    • Further research into molecular mechanisms can guide therapeutic strategies.