Complement factor H serum levels determine resistance to pneumococcal invasive disease

Erika Van Der Maten, Dineke Westra, Saskia Van Selm, Jeroen D. Langereis, Hester J. Bootsma, Fred J.H. Van Opzeeland, Ronald De Groot, Marieta M. Ruseva, Matthew C. Pickering, Lambert P.W.J. Van Den Heuvel, Nicole C.A.J. Van De Kar, Marien I. De Jonge, Michiel Van Der Flier*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

7 Citations (Scopus)

Abstract

Streptococcus pneumoniae is a major cause of life-threatening infections. Complement activation plays a vital role in opsonophagocytic killing of pneumococci in blood. Initial complement activation via the classical and lectin pathways is amplified through the alternative pathway amplification loop. Alternative pathway activity is inhibited by complement factor H (FH). Our study demonstrates the functional consequences of the variability in human serum FH levels on host defense. Using an in vivo mouse model combined with human in vitro assays, we show that the level of serum FH correlates with the efficacy of opsonophagocytic killing of pneumococci. In summary, we found that FH levels determine a delicate balance of alternative pathway activity, thus affecting the resistance to invasive pneumococcal disease. Our results suggest that variation in FH expression levels, naturally occurring in the human population, plays a thus far unrecognized role in the resistance to invasive pneumococcal disease.

Original languageEnglish
Pages (from-to)1820-1827
Number of pages8
JournalJournal of Infectious Diseases
Volume213
Issue number11
DOIs
Publication statusPublished - 1 Jun 2016
Externally publishedYes

Keywords

  • Alternative pathway
  • C3 opsonization
  • Complement system
  • Factor H
  • Invasive pneumococcal disease
  • Streptococcus pneumoniae

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