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Serum amyloid P aids complement-mediated immunity to Streptococcus pneumoniae.

Jose Yuste1, Marina Botto, Stephen E Bottoms

  • 1Centre for Respiratory Research, Department of Medicine, Royal Free and University College Medical School, Rayne Institute, London, United Kingdom.

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Summary

Serum amyloid P (SAP) is crucial for innate immunity against Streptococcus pneumoniae. SAP enhances complement deposition and phagocytosis, protecting against fatal pneumonia in mice.

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Area of Science:

  • Immunology
  • Microbiology
  • Biochemistry

Background:

  • The physiological roles of serum amyloid P (SAP), an acute phase protein, are not fully understood.
  • SAP deficiency has not been naturally observed, suggesting a vital function.

Purpose of the Study:

  • To investigate the role of SAP in innate immunity against the human pathogen Streptococcus pneumoniae.
  • To elucidate SAP's contribution to host defense mechanisms.

Main Methods:

  • Flow cytometry assays were employed to analyze SAP's interaction with S. pneumoniae.
  • Complement deposition and phagocytosis efficiency were measured.
  • SAP-deficient and wild-type mouse models were used to study pneumonia outcomes.

Main Results:

  • SAP binds to S. pneumoniae, enhancing classical complement pathway deposition.
  • SAP significantly improves the phagocytosis of S. pneumoniae.
  • SAP-deficient mice exhibited impaired inflammatory response, uncontrolled bacterial replication, and fatal pneumonia.
  • Complementation with human SAP restored complement deposition, phagocytosis, and survival in SAP-deficient mice.

Conclusions:

  • SAP plays a critical, physiologically significant role in complement-mediated immunity against Streptococcus pneumoniae.
  • SAP is essential for controlling bacterial pneumonia and ensuring survival.
  • These findings underscore the importance of the classical complement pathway in innate immunity.