Related Experiment Video
Updated: Jul 15, 2026

Depletion of Specific Cell Populations by Complement Depletion
Published on: February 5, 2010
Influence of a deficiency of the second component of complement on the bactericidal activity of neutrophils in vitro
Abstract:
Serum from three patients with a complete, selective deficiency of the second component of complement (C2) did not promote optimal killing of Staphylococcus aureus, 502A by neutrophilic polymorphonuclear leukocytes (PMN) in vitro. The addition of C2 reagent or the presence of heat-stable opsonin in the C2-deficient serum corrected the defective killing of S. aureus that was observed with patient or control PMN. PMN from the patients or control subjects killed bacteria with equal efficiency under conditions of optimal opsonization (normal pooled serum). However, twice-washed control PMN were better than patient PMN in killing S. aureus under circumstances of suboptimal opsonization (C2-deficient serum, heated C2-deficient serum, heated normal pooled serum, or no replacement of serum). The latter finding was due to residual C2 on the surface of twice-washed control cells. As repeated washing of control PMN progressively removed cell-associated C2, the staphylocidal effectiveness of the control RMN decreased to the level of patient PMN. In contrast to the findings with S. aureus, triply-washed PMN from patients or controls killed normal numbers of Escherichia coli, ON2, in C2-deficient serum.
Insights
Patients with a complete deficiency of the second component of complement (C2) show impaired killing of Staphylococcus aureus by neutrophils. This defect is linked to insufficient C2 for optimal opsonization, highlighting C2
Area of Science:
- Immunology
- Microbiology
- Complement System
Background:
- The second component of complement (C2) plays a crucial role in the immune response.
- Polymorphonuclear leukocytes (PMN) are key phagocytic cells in bacterial killing.
- Deficiencies in complement components can impair host defense against infections.
Purpose of the Study:
- To investigate the role of C2 in the opsonophagocytic killing of Staphylococcus aureus by human PMN.
- To determine the impact of C2 deficiency on PMN function in vitro.
- To assess the contribution of cell-associated C2 to bacterial clearance.
Main Methods:
- Utilized serum from C2-deficient patients and healthy controls.
- Assayed the killing of Staphylococcus aureus (502A) by PMN in vitro under various opsonization conditions.
- Investigated the effect of C2 reagent addition and serum heating on bacterial killing.
- Examined the role of PMN washing on bacterial clearance.
Main Results:
- C2-deficient serum resulted in suboptimal killing of S. aureus by PMN.
- Addition of C2 reagent or heat-stable opsonins corrected the defective bacterial killing.
- Twice-washed control PMN showed enhanced S. aureus killing compared to patient PMN, attributed to residual C2.
- Progressive washing of control PMN reduced their staphylocidal effectiveness.
- PMN from both C2-deficient patients and controls effectively killed Escherichia coli in C2-deficient serum.
Conclusions:
- A complete, selective deficiency of C2 impairs the optimal killing of Staphylococcus aureus by PMN.
- C2 is essential for efficient opsonization and subsequent phagocytosis and killing of S. aureus.
- Cell-associated C2 on PMN contributes to bacterial clearance, particularly under suboptimal opsonization conditions.
- The complement system's role in bacterial killing may vary depending on the bacterial species.
More Related Videos
07:28Standardized In vitro Assays to Visualize and Quantify Interactions between Human Neutrophils and Staphylococcus aureus Biofilms
Published on: June 8, 2022
14:05Morphological and Compositional Analysis of Neutrophil Extracellular Traps Induced by Microbial and Chemical Stimuli
Published on: November 4, 2022
Related Concept Videos
Antimicrobial Proteins
Interferons
Interferons (IFNs) are proteins produced by lymphocytes, macrophages, and fibroblasts infected with viruses. While IFNs cannot prevent viruses from entering and...
Complement System
Determinants of Bacterial Pathogenicity and Virulence