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C-reactive protein: structural biology and host defense function.

A J Szalai1, A Agrawal, T J Greenhough

  • 1Department of Medicine, University of Alabama at Birmingham, 35294-0006, USA. rheu022@uabdpo.dpo.uab.edu

Clinical Chemistry and Laboratory Medicine
|June 3, 1999
PubMed
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Human C-reactive protein (CRP) acts as a host defense molecule. Studies in transgenic mice show CRP significantly reduces mortality and bacterial load when infected with Streptococcus pneumoniae, highlighting its crucial role in fighting infections.

Area of Science:

  • Biochemistry
  • Immunology
  • Structural Biology

Background:

  • Human C-reactive protein (CRP) is a calcium-binding acute phase protein specific for phosphocholine.
  • Structural and mutagenesis studies have elucidated CRP's molecular architecture and function.
  • Transgenic mouse models have been instrumental in confirming CRP's role in host defense.

Purpose of the Study:

  • To investigate the host defense functions of human C-reactive protein (CRP) using transgenic mice.
  • To determine the impact of CRP on mortality and bacterial load during Streptococcus pneumoniae infection.

Main Methods:

  • Utilized human C-reactive protein transgenic mice for infection studies.
  • Assessed lifespan and mortality rates in infected transgenic and wild-type mice.

Related Experiment Videos

  • Quantified bacteremia levels to evaluate CRP's effect on bacterial clearance.

    • Main Results:

    • Transgenic mice expressing human CRP exhibited increased lifespan and reduced mortality compared to wild-type controls when infected with Streptococcus pneumoniae.
    • A significant reduction (up to 400-fold) in bacteremia was observed in CRP-expressing mice.
    • Both complement-dependent and complement-independent mechanisms contributed to the host-protective effects of CRP.

    Conclusions:

    • Human C-reactive protein plays a vital role in host defense against Streptococcus pneumoniae infection.
    • CRP confers protection through both complement-mediated and independent pathways.
    • Targeting CRP may represent a therapeutic strategy for bacterial infections.