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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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Inflammatory Response I: Vascular and Cellular01:30

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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,...
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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.
Interferons
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Inflammatory Response01:28

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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.
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Factors Affecting the Risk of Infection01:26

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The hosts' susceptibility to infection depends on several factors. The integrity of the skin and mucous membranes helps protect the body against microbial attacks. When the skin is altered, the chance of infection, limb loss, and even death increases.
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Updated: Aug 4, 2025

Intravenous Endotoxin Challenge in Healthy Humans: An Experimental Platform to Investigate and Modulate Systemic Inflammation
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Hyper-inflammation and complement in COVID-19.

Bruno G Pires1, Rodrigo T Calado1

  • 1Department of Medical Imaging, Hematology, and Oncology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.

American Journal of Hematology
|March 31, 2023
PubMed
Summary
This summary is machine-generated.

Severe COVID-19 involves hyperinflammation driven by complement over-activation. Therapeutic complement inhibition may help, with upstream targeting showing promise for blocking inflammation effectively.

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Area of Science:

  • Immunology
  • Virology
  • Pathobiology

Background:

  • COVID-19 presents a wide spectrum of severity, with hyperinflammation and complement system over-activation playing key roles in severe cases.
  • The SARS-CoV-2 virus can directly activate the complement system through multiple pathways, contributing to disease severity.
  • Intracellular complement activation (the complesome) within infected cells is also implicated in COVID-19 pathogenesis.

Purpose of the Study:

  • To explore the role of complement system over-activation in severe COVID-19.
  • To evaluate the potential therapeutic benefits of complement inhibition in COVID-19 patients.
  • To understand the mechanisms by which SARS-CoV-2 interacts with the complement system.

Main Methods:

  • Review of existing literature on COVID-19, complement biology, and therapeutic strategies.
  • Analysis of data from early-phase clinical trials (Phase I and II) investigating complement inhibitors.
  • Hypothesizing optimal targets and timing for complement inhibition based on pathway knowledge.

Main Results:

  • Complement over-activation is strongly associated with COVID-19 severity, microangiopathy, and hypercoagulability.
  • Early clinical trials show promising but conflicting results for complement inhibition therapies.
  • Upstream complement cascade inhibition is proposed as a potentially more effective strategy to block hyperinflammation.

Conclusions:

  • Complement system dysregulation is central to severe COVID-19.
  • Targeting the complement system therapeutically holds potential for treating severe COVID-19.
  • Further randomized controlled trials (Phase III) are necessary to confirm efficacy and optimal strategies for complement inhibition.