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Related Concept Videos

Complement System01:27

Complement System

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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...
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Antimicrobial Proteins01:23

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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.
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Defense Against Bacterial Pathogens01:31

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The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
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Nursing Clinical Information System01:27

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Nursing Clinical Information System (NCIS)
A Nursing Clinical Information System (NCIS) is a specialized type of healthcare information system tailored to meet the unique needs of nursing practice. It incorporates the principles of nursing informatics to streamline information management and improve the quality of care delivery.
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Combined Effects of Drugs: Synergism01:27

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Synergism is a useful mechanism where combining two or more drugs is more effective than each constituent used alone. Such combinations are also called supra-additive interactions. The drugs collectively enhance the final therapeutic effect by acting on different targets. Another advantage is that the low dose of each constituent drug is sufficient to achieve the desired effect. This helps reduce the duration of therapy and lower the adverse effects of these drugs.
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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.
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Related Experiment Video

Updated: Dec 16, 2025

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

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Complement in sepsis-when science meets clinics.

Tom E Mollnes1,2,3,4, Markus Huber-Lang5

  • 1Research Laboratory, Nordland Hospital Bodø, Bodø, Norway.

FEBS Letters
|July 5, 2020
PubMed
Summary
This summary is machine-generated.

Sepsis causes organ dysfunction, challenging the immune system. Targeting complement and Toll-like receptors early offers a promising "upstream approach" to re-establish immune balance and improve patient outcomes.

Keywords:
C3aC5aToll-like receptorscomplement activationsepsistherapy

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Area of Science:

  • Immunology
  • Infectious Diseases
  • Critical Care Medicine

Background:

  • Sepsis, a life-threatening organ dysfunction due to infection, poses a significant challenge to the immune system.
  • The complement system, a key part of innate immunity, has been studied in sepsis, but its clinical application is limited.
  • Complement activation products (C3a, C5a) and their receptors are potential diagnostic markers and therapeutic targets.

Purpose of the Study:

  • To investigate the translational value of the complement system in sepsis.
  • To explore therapeutic strategies beyond monotherapy for sepsis management.
  • To propose an "upstream approach" targeting early innate immune recognition in sepsis.

Main Methods:

  • Review of complement system's role in various sepsis models.
  • Analysis of sepsis-induced interactions between complement, coagulation, and fibrinolytic cascades.
  • Proposal for patient-tailored combined therapies, including complement and Toll-like receptor inhibition.

Main Results:

  • Monotherapy with complement inhibitors may be insufficient to reverse complex sepsis mechanisms.
  • Sepsis involves 'thromboinflammation' due to dysregulated immune cascades, leading to multi-organ failure.
  • Early inhibition of innate immune recognition systems is hypothesized to prevent irreversible inflammatory responses.

Conclusions:

  • Reliable monitoring of complement function is crucial for sepsis management.
  • Patient-tailored combined therapies, like "upstream approach" targeting complement and Toll-like receptors, are promising.
  • This strategy aims to block early innate immune activation before widespread inflammation and organ damage occur.