Related Experiment Video
Updated: Jul 24, 2026
06:29
Methods for Quantitative Detection of Antibody-induced Complement Activation on Red Blood Cells
Published on: January 29, 2014
Complement-dependent acute-phase expression of C-reactive protein and serum amyloid P-component
A J Szalai1, F W van Ginkel, Y Wang
1Division of Clinical Immunology and Rheumatology, Department of Microbiology, University of Alabama, Birmingham, AL 35294, USA. Alex.Szalai@ccc.uab.edu
Journal of Immunology (Baltimore, Md. : 1950)
|July 6, 2000
Summary
Complement activation product C5a, working with IL-6 and IL-1beta, boosts acute-phase protein production during the acute-phase response. This study clarifies the in vivo role of complement in regulating these crucial inflammatory proteins.
Area of Science:
- Immunology
- Complement System Biology
- Inflammation Research
Background:
- The acute-phase response (APR) involves cytokines like TNF-alpha, IL-1beta, and IL-6.
- Anaphylotoxin C5a, from complement activation, induces cytokine and acute-phase protein synthesis in vitro.
- The in vivo role of C5a in APR regulation remains unclear.
Purpose of the Study:
- To investigate the role of complement activation in inducing acute-phase proteins CRP and SAP in vivo.
- To determine if C5a contributes to the regulation of the acute-phase response.
Main Methods:
- Utilized human C-reactive protein (CRP) transgenic mice deficient in C3 or C5.
- Administered lipopolysaccharide (LPS) and cobra venom factor to activate complement.
- Injected recombinant human C5a into transgenic mice, including IL-6 deficient models.
Main Results:
- Absence of C3 or C5 reduced LPS-induced CRP and SAP up-regulation.
- LPS induced IL-1beta and IL-6 in normal mice, but only IL-6 in complement-deficient mice.
- C5a injection elevated CRP and SAP, but only in the presence of IL-6.
Conclusions:
- Complement activation, specifically C5a, plays a significant role in the in vivo acute-phase response.
- C5a acts in concert with IL-6 and/or IL-1beta to up-regulate CRP and SAP genes.
- This research elucidates a key mechanism linking complement activation to inflammatory protein production.
More Related Videos
Related Concept Videos
01:27Complement 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...
01:19Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers
Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
01:26Acute Inflammation I: Inflammatory Response
Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...
01:25Acute 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...
01:19Hypersensitivity 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...