Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Pneumococcal surface protein A inhibits complement activation by Streptococcus pneumoniae.

A H Tu1, R L Fulgham, M A McCrory

  • 1Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.

Infection and Immunity
|August 24, 1999
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Pneumococcal Vaccines.

Microbiology spectrum·2019
Same author

Deficits in episodic memory are related to uncontrolled eating in a sample of healthy adults.

Appetite·2017
Same author

The role of genetic variants in CRP in radiographic severity in African Americans with early and established rheumatoid arthritis.

Genes and immunity·2015
Same author

Nanogel-based pneumococcal surface protein A nasal vaccine induces microRNA-associated Th17 cell responses with neutralizing antibodies against Streptococcus pneumoniae in macaques.

Mucosal immunology·2015
Same author

Complement C3 activation in cyst fluid and urine from autosomal dominant polycystic kidney disease patients.

Journal of internal medicine·2014
Same author

C-reactive protein induces expression of tissue factor and plasminogen activator inhibitor-1 and promotes fibrin accumulation in vein grafts.

Journal of thrombosis and haemostasis : JTH·2014

Pneumococcal surface protein A (PspA) hinders the immune system's complement pathway, allowing Streptococcus pneumoniae to evade clearance. PspA's interference with complement deposition is key to its role in pneumococcal virulence.

Area of Science:

  • Immunology
  • Microbiology
  • Molecular Biology

Background:

  • Pneumococcal surface protein A (PspA) is a key virulence factor of Streptococcus pneumoniae.
  • Understanding PspA's role in immune evasion is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the mechanism by which PspA contributes to Streptococcus pneumoniae virulence.
  • To determine how PspA interacts with the host complement system.

Main Methods:

  • Infection of wild-type and complement-deficient mice (C3, C5, factor B) with PspA-expressing and PspA-deficient pneumococci.
  • Analysis of serum complement activation and bacterial clearance in vivo.
  • In vitro opsonization assays with immunoblots to assess C3b deposition and C3 convertase formation.

Related Experiment Videos

Main Results:

  • PspA-expressing pneumococci showed no significant complement depletion and were not cleared rapidly from blood.
  • PspA-deficient pneumococci induced significant complement activation and were cleared within 6 hours.
  • In C3- or factor B-deficient mice, PspA-negative pneumococci became virulent, while in C5-deficient mice, they remained avirulent.
  • In vitro, PspA inhibited C3b deposition and C3 convertase formation on pneumococci.

Conclusions:

  • PspA interferes with complement-dependent host defense mechanisms, particularly those involving factor B.
  • PspA likely functions by inhibiting C3b deposition and/or alternative pathway C3 convertase formation.
  • This interference reduces bacterial clearance mediated by complement receptors, enhancing pneumococcal virulence.