Related Experiment Video

Updated: Sep 26, 2026

Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery
10:03

Inducing Meningococcal Meningitis Serogroup C in Mice via Intracisternal Delivery

Published on: November 5, 2019

Antibody-dependent killing of meningococci by human neutrophils in serum of late complement component-deficient

Alexander E Platonov1, Irina V Vershinina, Helena Käyhty

  • 1Central Institute of Epidemiology, Moscow, Russia. platonov@pcr.ru

International Archives of Allergy and Immunology
|May 13, 2003
PubMed
Abstract

Insights

Vaccination enhances the ability of neutrophils to kill meningococci in patients with late complement component deficiency (LCCD). This improved bacterial killing capacity, dependent on antibodies and complement, offers protection against meningococcal infections.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Vaccinology

Background:

  • Late complement component deficiency (LCCD) patients experienced recurrent meningococcal infections.
  • Thirty-one LCCD patients were vaccinated with a quadrivalent meningococcal polysaccharide vaccine (A+C+W135+Y).
  • The study investigated the role of human neutrophils (PMNL) in killing meningococci in LCCD patients.

Purpose of the Study:

  • To assess the impact of meningococcal vaccination on the ability of PMNL to kill meningococci in LCCD patients.
  • To determine the correlation between specific antibody levels and PMNL-mediated bacterial killing.
  • To elucidate the mechanism of protection conferred by vaccination in LCCD individuals.

Main Methods:

  • Meningococci (serogroups A and W135) were incubated with LCCD patient sera, with and without PMNL.
  • Bacterial viability was quantified by colony-forming unit (CFU) counts after incubation.
  • Sera were collected pre-vaccination and at various time points post-vaccination (1 month to 3 years).

Main Results:

  • PMNL effectively killed meningococci in LCCD sera post-vaccination, unlike in prevaccination sera where bacteria grew.
  • Effective PMNL-mediated killing increased significantly from 40% pre-vaccination to 80% within 1 year post-vaccination (p < 0.05).
  • Killing rates correlated with higher concentrations of serogroup-specific immunoglobulins, with 83% of sera having >5 µg/ml anti-group A antibodies promoting killing.

Conclusions:

  • Human neutrophils kill meningococci in the presence of LCCD serum, an effect enhanced by vaccination.
  • Vaccination-induced protection against meningococcal disease in LCCD patients is likely mediated by increased PMNL killing capacity.
  • This PMNL-mediated killing is dependent on both specific antibodies and complement activation.

More Related Videos

Induction of Leptomeningeal Cells Modification Via Intracisternal Injection05:55

Induction of Leptomeningeal Cells Modification Via Intracisternal Injection

Published on: May 7, 2020

Humanized Mouse Model to Study Bacterial Infections Targeting the Microvasculature11:40

Humanized Mouse Model to Study Bacterial Infections Targeting the Microvasculature

Published on: April 1, 2014

Related Concept Videos

Complement System01:27

Complement 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...
Hypersensitivity Reactions: Cytolytic Reactions01:01

Hypersensitivity Reactions: Cytolytic Reactions

Type II hypersensitivity involves IgG and IgM antibodies targeting cell surface antigens, leading to cell destruction. This can occur through complement activation, antibody-dependent cell-mediated cytotoxicity (ADCC), or acting as opsonins for phagocytosis. When excessive, these reactions cause significant tissue damage.Drug-induced hemolytic anemia is a common example, where drugs like penicillin or cephalosporins bind to red blood cells, forming drug-protein complexes. These complexes...
Bacterial Meningitis01:24

Bacterial Meningitis

Bacterial meningitis is a severe infectious disease involving inflammation of the meninges, the protective membranes surrounding the brain and spinal cord. It occurs when pathogenic bacteria cross the blood–brain barrier and enter the cerebrospinal fluid. Common causative organisms include Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae type b, Listeria monocytogenes, and Escherichia coli K1. The exact route of entry varies by pathogen and host condition.Routes of Entry...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

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...
Antibody Actions01:26

Antibody Actions

Antibodies, or immunoglobulins, are critical players in the immune system's arsenal against invading pathogens. Produced by B cells and plasma cells, their primary role is to detect and bind to specific antigens, molecules found on the surface of pathogens like bacteria or viruses. Beyond antigen recognition, antibodies perform several vital functions that contribute to immune defense.
Neutralization
Antibodies can bind to pathogens, preventing them from infecting host cells. This process...
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...