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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...
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,...
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 II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the exudate's...
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

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A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats
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Published on: February 20, 2021

The systemic pro-inflammatory response in sepsis.

Hanna Katrien de Jong1, Tom van der Poll, Willem Joost Wiersinga

  • 1Center for Molecular Medicine, University of Amsterdam, Amsterdam, The Netherlands.

Journal of Innate Immunity
|June 10, 2010
PubMed
Summary
This summary is machine-generated.

Systemic inflammatory response syndrome (SIRS), a hallmark of sepsis, involves cytokines, plasma cascades, and cellular responses. Understanding these complex interactions is key to developing new sepsis treatments.

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Last Updated: Jun 12, 2026

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats
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Evaluation of a Reliable Biomarker in a Cecal Ligation and Puncture-Induced Mouse Model of Sepsis
05:28

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Published on: December 9, 2022

Cecal Ligation Puncture Procedure
11:53

Cecal Ligation Puncture Procedure

Published on: May 7, 2011

Area of Science:

  • Immunology
  • Pathophysiology
  • Molecular Biology

Background:

  • Systemic inflammatory response syndrome (SIRS) is a critical host response to pathogens, central to sepsis.
  • Key molecular and cellular components include cytokines, plasma cascades, acute-phase proteins, leukocytes, and endothelium.
  • High-throughput genetic studies reveal novel pro-inflammatory cytokine network players in sepsis.

Purpose of the Study:

  • To elucidate the complex molecular and cellular mechanisms underlying SIRS in sepsis.
  • To identify key mediators and pathways involved in the inflammatory and coagulation crosstalk during sepsis.
  • To highlight the role of the complement system, particularly C5a, in sepsis pathogenesis.

Main Methods:

  • Review of high-throughput genetic profiling studies.
  • Analysis of molecular components: cytokines, plasma cascades, acute-phase proteins.
  • Examination of cellular components: leukocytes and endothelium.
  • Investigation of the interplay between inflammation, coagulation, and complement systems.

Main Results:

  • Identified novel pro-inflammatory cytokines: IL-17, HMGB1, MIF, Mrp8/14, and TREM-1.
  • Confirmed universal activation of coagulation and downregulation of anticoagulant/fibrinolytic systems in septic SIRS.
  • Demonstrated significant cross-talk between inflammation and coagulation via protease-activated receptors.
  • Highlighted excessive complement system activation, with C5a playing a crucial role.

Conclusions:

  • Sepsis involves a complex interplay of host-pathogen interactions, cytokine networks, coagulation, and complement systems.
  • Understanding these multidirectional interactions is essential for identifying new therapeutic targets.
  • Modulating the excessive activation of these interconnected systems offers a promising avenue for sepsis treatment.