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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...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...
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...
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
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...

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Pseudofracture: An Acute Peripheral Tissue Trauma Model
10:08

Pseudofracture: An Acute Peripheral Tissue Trauma Model

Published on: April 18, 2011

Early complementopathy after multiple injuries in humans.

Anne-Maud Burk1, Myriam Martin, Michael A Flierl

  • 1Department of Traumatology, Hand-, Plastic-, and Reconstructive Surgery, University Hospital Ulm, Ulm, Germany.

Shock (Augusta, Ga.)
|January 20, 2012
PubMed
Summary
This summary is machine-generated.

Multiple trauma causes immediate complement cascade activation and dysfunction in humans, leading to a "complementopathy." This early immune dysfunction impacts innate immunity and is linked to patient outcomes.

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Depletion of Specific Cell Populations by Complement Depletion
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Depletion of Specific Cell Populations by Complement Depletion
06:17

Depletion of Specific Cell Populations by Complement Depletion

Published on: February 5, 2010

Area of Science:

  • Immunology
  • Trauma Medicine
  • Biochemistry

Background:

  • Severe tissue injury triggers a systemic inflammatory response via innate immunity.
  • The immediate effects of multiple trauma on early human complement function remain largely unknown.

Purpose of the Study:

  • To investigate the hypothesis that multiple trauma causes immediate complement cascade activation, consumption, and dysfunction.
  • To determine if this
  • complementopathy
  • is associated with patient morbidity and mortality.

Main Methods:

  • Prospective multicenter study involving 25 healthy volunteers and 40 polytrauma patients.
  • Serum complement profiles analyzed at multiple time points post-trauma (scene, ER admission, 4, 12, 24, 120, 240 hours).
  • Assessed complement hemolytic activity (CH-50), activation products (C3a, C5a), terminal complex (SC5b-9), mannose-binding lectin, and fluid-phase inhibitors (C4b-binding protein, factor I).

Main Results:

  • Complement hemolytic activity (CH-50) significantly reduced within 24 hours, recovering by day 5, and predicting 28-day survival.
  • Elevated C3a and C5a levels correlated with traumatic brain injury severity and survival.
  • Complement activation products showed rapid increases, while key inhibitors decreased early post-trauma.

Conclusions:

  • Multiple trauma induces rapid, synchronized complement activation and dysfunction, termed
  • complementopathy
  • .
  • This early complementopathy may contribute to the impaired innate immune response observed after severe trauma.
  • Findings suggest complement system dysregulation is a critical early event in polytrauma patients.