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

Complement System01:27

Complement System

10.6K
The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
10.6K
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
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

10.9K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
10.9K
Coagulation01:09

Coagulation

8.4K
The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
8.4K
Coagulation01:06

Coagulation

1.5K
Colloidal solids are solid particles suspended in solution. They are usually negatively charged, attracting a compact primary layer of positively charged ions, which attract more counterions to form an electrical double layer. Electrostatic repulsion between the charged double layers prevents the particles from colliding, stabilizing the colloids. These solids are often undesirable because they can contain toxins that are difficult to remove. Coagulation is a technique that helps aggregate and...
1.5K
Introduction to Hemostasis01:05

Introduction to Hemostasis

14.2K
Hemostasis is a complex physiological process that prevents excessive bleeding when a blood vessel is injured. It's crucial for maintaining the integrity of the circulatory system, as it ensures that our blood remains fluid while still within the vascular network and yet clots to prevent blood loss upon vessel injury.
The three phases of hemostasis involve many clotting factors present in plasma and several substances released by platelets and injured tissue cells. It is a fast, localized,...
14.2K

You might also read

Related Articles

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

Sort by
Same author

Anthrax toxins exacerbate sepsis-induced coagulopathy and endothelial dysfunction in a baboon model of anthrax.

Journal of thrombosis and haemostasis : JTH·2025
Same author

Bacterial infection and activation of the contact pathway of coagulation.

Blood vessels, thrombosis & hemostasis·2025
Same author

Common Gene Networks Orchestrate Organelle Architecture and Inter-Organelle Metabolic Flows for Mucin Production in High Endothelial and Goblet Cells.

bioRxiv : the preprint server for biology·2025
Same author

Multimodal Analysis of Sepsis-induced Cardiomyopathy in a Baboon Model.

bioRxiv : the preprint server for biology·2025
Same author

Protective effects of factor XI inhibition by abelacimab in a baboon model of live Staphylococcus aureus sepsis.

Journal of thrombosis and haemostasis : JTH·2025
Same author

S1PR1 regulates lymphatic valve development and tertiary lymphoid organ formation in the ileum.

The Journal of experimental medicine·2025
Same journal

Apoptotic versus procoagulant platelets: similar "necrotic" phenotype and procoagulant activity in vitro, but distinct adhesive protein composition.

Thrombosis research·2026
Same journal

Heatstroke-induced coagulopathy: A scoping review of therapeutic strategies and outcome reporting.

Thrombosis research·2026
Same journal

Mapping thrombus habitat: Non-contrast MRI radiomics and pixel-tile histomics approach to track venous thrombosis evolution in mice.

Thrombosis research·2026
Same journal

A study protocol for a randomised controlled trial evaluating the safety and efficiency of the YEARS algorithm versus computed tomography pulmonary angiography only for suspected acute pulmonary embolism in patients with cancer: the Hydra Study.

Thrombosis research·2026
Same journal

Associating the phenotypic expression of platelets with disease type through image-based single-cell profiling.

Thrombosis research·2026
Same journal

The mechanisms of contractile dysfunction following chronic limited platelet activation in (pro)thrombotic conditions.

Thrombosis research·2026
See all related articles

Related Experiment Video

Updated: Apr 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

9.4K

Crosstalk between the coagulation and complement systems in sepsis.

Florea Lupu1, Ravi S Keshari1, John D Lambris2

  • 1Cardiovascular Biology, Research Programs, Oklahoma Medical Research Foundation, Oklahoma City, OK.

Thrombosis Research
|April 25, 2014
PubMed
Summary
This summary is machine-generated.

Sepsis triggers complement and coagulation systems, leading to organ damage. Inhibiting complement activation with compstatin reduced sepsis complications, suggesting a potential therapeutic strategy for severe sepsis.

Keywords:
CoagulationComplementDisseminated intravascular coagulationInflammationMultiple organ failureSepsis

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

3.7K
Cecal Ligation Puncture Procedure
11:53

Cecal Ligation Puncture Procedure

Published on: May 7, 2011

55.2K

Related Experiment Videos

Last Updated: Apr 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

9.4K
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

3.7K
Cecal Ligation Puncture Procedure
11:53

Cecal Ligation Puncture Procedure

Published on: May 7, 2011

55.2K

Area of Science:

  • Immunology
  • Hematology
  • Microbiology

Background:

  • Sepsis activates hemostatic and complement systems, causing tissue damage and organ failure.
  • Uncontrolled systemic activation of these cascades is a hallmark of severe sepsis.

Purpose of the Study:

  • To investigate the role of complement and coagulation activation in experimental sepsis.
  • To evaluate the therapeutic potential of a complement inhibitor in sepsis.

Main Methods:

  • Experimental sepsis was induced in baboons using live bacteria (E. coli, S. aureus, B. anthracis) or peptidoglycan.
  • Compstatin, a C3 convertase inhibitor, was administered to assess its effects on sepsis markers.
  • Hemostatic and complement activation markers were monitored.

Main Results:

  • Bacterial challenges rapidly induced disseminated intravascular coagulation and complement activation.
  • Compstatin treatment prevented complement activation, reduced thrombocytopenia, and mitigated coagulopathy.
  • Endothelial anticoagulant properties were preserved with compstatin therapy.

Conclusions:

  • Live bacteria and bacterial products activate complement and coagulation cascades during sepsis.
  • Blocking complement activation, particularly during organ failure, is a promising therapeutic strategy for severe sepsis.