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Related Concept Videos

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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...
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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...
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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...
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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...
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Related Experiment Video

Updated: Jul 4, 2026

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

Functions of the complement components C3 and C5 during sepsis.

Michael A Flierl1, Daniel Rittirsch, Brian A Nadeau

  • 1Dept. of Pathology, University of Michigan Medical School, 1301 Catherine Rd, Ann Arbor, MI 48109, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|July 1, 2008
PubMed
Summary

Complement C3 is vital for controlling bacteria during sepsis, while C5 plays a lesser role. Blocking C5a, not C5, may offer a better therapeutic strategy by preserving the membrane attack complex.

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

Published on: June 15, 2019

Related Experiment Videos

Last Updated: Jul 4, 2026

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

Cecal Ligation Puncture Procedure
11:53

Cecal Ligation Puncture Procedure

Published on: May 7, 2011

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

Area of Science:

  • Immunology
  • Pathogenesis of Sepsis

Background:

  • The complement system's role in sepsis pathogenesis is crucial but not fully understood.
  • Specific complement components like C3 and C5 require further investigation in sepsis models.

Purpose of the Study:

  • To investigate the distinct roles of complement C3 and C5 in sepsis-induced mortality and bacteremia.
  • To evaluate the impact of C3 and C5 deficiency on the formation of the membrane attack complex (MAC) and inflammatory responses.

Main Methods:

  • Utilized a cecal ligation and puncture (CLP) sepsis model in wild-type, C3-deficient, and C5-deficient mice.
  • Assessed survival rates, plasma inflammatory mediator levels, bacterial loads (bacteremia), and MAC formation (via CH-50 assays).

Main Results:

  • C3-deficient mice exhibited significantly reduced survival and decreased pro-inflammatory mediators compared to wild-type.
  • C5-deficient mice showed similar survival to wild-type but had a drastically higher increase in bacteremia.
  • Septic C3-deficient mice showed increased MAC formation, contrasting with negative controls, while C5-deficient mice were unable to form the MAC.

Conclusions:

  • Hemolytic complement activity, particularly involving C3, is essential for controlling bacteremia in sepsis.
  • Targeting C5a or its receptors, rather than C5 itself, presents a more promising therapeutic approach for sepsis, allowing MAC formation while mitigating C5a's adverse effects.