Related Experiment Video
Updated: Jun 23, 2026

Humanized Mouse Model to Study Bacterial Infections Targeting the Microvasculature
Published on: April 1, 2014
Factor H and neisserial pathogenesis
1Children's Hospital Oakland Research Institute, Oakland, CA, USA.
Abstract:
Both Neisseria gonorrhoeae and N. meningitidis bind to factor H which enhances their ability to evade complement-dependent killing. While porin is the ligand for human fH on gonococci, meningococci use a lipoprotein called factor H binding protein (fHbp) to bind to factor H and enhance their ability to evade complement-dependent killing. This protein is currently being intensively investigated as a meningococcal vaccine candidate antigen. Consistent with the observation that meningococci cause natural infection only in humans, the organism resists human complement, and are more readily killed by complement from lower animals. This human species-specific complement evasion has important implications for evaluation of vaccine-elicited antibodies using non-human complement sources and development of animal models of disease.
Insights
Neisseria meningitidis uses factor H binding protein (fHbp) to evade human complement killing, impacting vaccine development. Understanding this interaction is crucial for effective meningococcal vaccines and accurate animal models.
Area of Science:
- Microbiology
- Immunology
- Vaccinology
Background:
- Neisseria gonorrhoeae and Neisseria meningitidis evade complement-dependent killing by binding to human factor H.
- While gonococci use porin, meningococci utilize factor H binding protein (fHbp) for factor H interaction.
Purpose of the Study:
- To investigate the role of fHbp in Neisseria meningitidis's evasion of complement.
- To highlight implications for meningococcal vaccine development and animal model studies.
Main Methods:
- Analysis of factor H binding mechanisms in Neisseria species.
- Investigation of complement resistance in relation to human and animal complement sources.
Main Results:
- Neisseria meningitidis employs fHbp to bind factor H, enhancing survival against complement-mediated lysis.
- Meningococci exhibit human-specific complement resistance, being more susceptible to animal complement.
Conclusions:
- fHbp is a key factor in meningococcal complement evasion and a promising vaccine antigen target.
- Species-specific complement evasion necessitates careful consideration for evaluating vaccine efficacy in animal models.
Related Concept Videos
Determinants of Bacterial Pathogenicity and Virulence
Extrinsic and Intrinsic Pathways of Hemostasis
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Encephalitis ll: Pathophysiology
Bacterial Meningitis II: Pathophysiology
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Clot Retraction and Fibrinolysis

