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Receptors1
,
Departments of
* Molecular Genetics and Microbiology and
Internal Medicine, School of Medicine, University of New Mexico, and
U.S. Department of Veterans Affairs Medical Center, Albuquerque, NM 87108
Streptococcus pneumoniae is an important human
pathogen and the most common cause of community-acquired pneumonia.
Both adaptive and innate immune mechanisms provide protection from
infection. Innate immunity to S. pneumoniae in mice is
mediated by naturally occurring anti-phosphocholine (PC) Abs and
complement. The human acute-phase reactant C-reactive protein (CRP)
also protects mice from lethal S. pneumoniae infection.
CRP and anti-PC Ab share the ability to bind to PC on the cell wall
C-polysaccharide of S. pneumoniae and to activate
complement. CRP and IgG anti-PC also bind to Fc
R. In this study,
FcR- and complement-deficient mice were used to compare the
mechanisms of protection conferred by CRP and anti-PC Ab. Injection
of CRP protected wild-type, FcR-chain-, FcRIIb-, and
FcRIII-deficient mice from infection. Complement was required for
the protective effect of CRP as cobra venom factor treatment eliminated
the effect of CRP in both -chain-deficient and wild-type mice, and
CRP failed to protect C3- or C4-deficient mice from infection.
Unexpectedly, -chain-deficient mice were extremely sensitive to
pneumococcal infection. This sensitivity was associated with low levels
of natural anti-PC Ab. -chain-deficient mice immunized with
nonencapsulated S. pneumoniae produced both IgM- and IgG
PC-specific Abs, were protected from infection, and were able to clear
the bacteria from the bloodstream. The protection provided by
immunization was eliminated by complement depletion. The results show
that in this model of systemic infection with highly virulent S.
pneumoniae, protection from lethality by CRP and anti-PC
Abs requires complement, but not FcR.
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