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Related Concept Videos

Complement System01:27

Complement System

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 membrane...
Antimicrobial Proteins01:23

Antimicrobial Proteins

Antimicrobial proteins are important components of the immune system. They aid the body in combating pathogens by either killing them directly or hindering their replication processes. Four main types of antimicrobial substances are interferons, the complement system, iron-binding proteins, and antimicrobial proteins.
Interferons
Interferons (IFNs) are proteins produced by lymphocytes, macrophages, and fibroblasts infected with viruses. While IFNs cannot prevent viruses from entering and...
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...
Complementation Tests00:49

Complementation Tests

A complementation test is a simple cross to identify whether the two mutations are located on the same gene or different genes. It was first performed by Edward Lewis in the 1940s while working on fruit flies. He developed the test to identify the location and arrangement of different mutations on chromosomes.
Organisms heterozygous for different mutations are crossed pairwise in all combinations. If present on different genes, the mutations can complement each other by providing the missing...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
Pathophysiology of Heart Failure01:17

Pathophysiology of Heart Failure

Heart failure (HF) is a progressive syndrome involving ventricles that leads to inadequate cardiac output. It can be classified based on location and output or ejection fraction. Ejection fraction (EF) is an essential measurement in the diagnosis and surveillance of HF. Reduced EF corresponds to systolic heart failure (HFrEF). However, HF with preserved ejection fraction (HFpEF) is becoming increasingly prevalent. Also known as diastolic HF, this form of HF is related to aging. The...

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Related Experiment Video

Updated: May 15, 2026

Depletion of Specific Cell Populations by Complement Depletion
06:17

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

Role of complement in multiorgan failure.

Daniel Rittirsch1, Heinz Redl, Markus Huber-Lang

  • 1Division of Trauma Surgery, Department of Surgery, University Hospital Zurich, Raemistrasse 100, 8091 Zurich, Switzerland. drittirsch@googlemail.com

Clinical & Developmental Immunology
|January 16, 2013
PubMed
Summary
This summary is machine-generated.

Multiorgan failure (MOF) is a major cause of death in sepsis and SIRS. Uncontrolled complement system activation drives inflammation and organ dysfunction in these critical conditions.

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Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

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Last Updated: May 15, 2026

Depletion of Specific Cell Populations by Complement Depletion
06:17

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Published on: February 5, 2010

Pseudofracture: An Acute Peripheral Tissue Trauma Model
10:08

Pseudofracture: An Acute Peripheral Tissue Trauma Model

Published on: April 18, 2011

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
06:29

Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells

Published on: January 29, 2014

Area of Science:

  • Immunology
  • Critical Care Medicine
  • Trauma Research

Background:

  • Multiorgan failure (MOF) is the primary cause of mortality in patients experiencing sepsis and severe trauma-induced systemic inflammatory response syndrome (SIRS).
  • The innate immune system, particularly the complement system, plays a pivotal role in the complex inflammatory cascade underlying these conditions.
  • Dysregulated complement activation leads to excessive generation of inflammatory mediators, contributing to systemic organ damage.

Purpose of the Study:

  • To review the intricate mechanisms of the inflammatory response in the pathogenesis of MOF.
  • To specifically elucidate the critical role of the complement system in sepsis and SIRS-associated MOF.
  • To provide a comprehensive overview of current understanding regarding complement's contribution to organ dysfunction.

Main Methods:

  • Literature review of studies focusing on inflammation, sepsis, SIRS, trauma, and multiorgan failure.
  • Analysis of research detailing complement system activation pathways and their consequences.
  • Synthesis of findings related to immune response modulation and organ system impact.

Main Results:

  • The complement system is a key driver of inflammation in sepsis and SIRS.
  • Excessive complement activation products correlate with the development of MOF.
  • Specific complement components and pathways are implicated in the dysfunction of various organ systems.

Conclusions:

  • Targeting complement system activation presents a potential therapeutic strategy for mitigating MOF in sepsis and SIRS.
  • Understanding the precise mechanisms of complement-mediated inflammation is crucial for developing effective interventions.
  • Further research into complement regulation is warranted to improve patient outcomes in critical care settings.