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Updated: Jun 4, 2026
A Novel In vitro Model for Studying the Interactions Between Human Whole Blood and Endothelium
Published on: November 21, 2014
Whole-blood model
1Department of Infectious Diseases ⇐p; Microbiology, Imperial College School of Medicine, London, UK.
Abstract:
Neisseria meningitidis is an obligate human pathogen. When it interacts with the host, it can establish a commensal relationship or can, on a minority of occasions, invade and cause systemic disease. Protection against systemic disease, particularly for serogroup A and C infections, has been equated with the presence of bactericidal antibody directed against the capsular polysaccharide (CPS) (1). In serogroup B infections, the CPS resembles host-cell moieties, is non-immunogenic, and does not induce protection (2). Hence other components of the bacterial-cell envelope, such as outer-membrane proteins (OMPs), and cellular mechanisms of host defense, such as phagocytosis, have been implicated in immunity to serogroup B infections (3,4).
Insights
Neisseria meningitidis can be harmless or cause disease. Immunity to serogroup B infections relies on outer-membrane proteins and phagocytosis, as its capsular polysaccharide is non-immunogenic.
Area of Science:
- Microbiology
- Immunology
- Pathogen Research
Background:
- Neisseria meningitidis is a human pathogen that can be commensal or invasive.
- Immunity to serogroup A and C is mediated by antibodies to capsular polysaccharide (CPS).
- Serogroup B's CPS is non-immunogenic due to resemblance to host moieties, necessitating alternative immunity mechanisms.
Purpose of the Study:
- To investigate alternative mechanisms of immunity against Neisseria meningitidis serogroup B infections.
- To explore the role of outer-membrane proteins (OMPs) in host defense.
- To understand the significance of cellular defense mechanisms like phagocytosis.
Main Methods:
- Analysis of bacterial cell envelope components.
- Investigation of host immune responses.
- Studies on phagocytic activity against Neisseria meningitidis.
Main Results:
- Capsular polysaccharide (CPS) of serogroup B is non-immunogenic.
- Outer-membrane proteins (OMPs) are implicated in immunity.
- Phagocytosis plays a role in host defense against serogroup B.
Conclusions:
- Immunity to Neisseria meningitidis serogroup B infections is not dependent on CPS antibodies.
- Outer-membrane proteins and phagocytosis are key components of the immune response.
- Further research into OMPs and phagocytosis is crucial for developing serogroup B vaccines.
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