Inflammasomes in Pneumococcal Infection: Innate Immune Sensing and Bacterial Evasion Strategies

Curr Top Microbiol Immunol. 2016;397:215-27. doi: 10.1007/978-3-319-41171-2_11.


Streptococcus pneumoniae frequently colonizes the upper respiratory tract of healthy individuals, but also commonly causes severe invasive infections such as community-acquired pneumonia and meningitis. One of the key virulence factors of pneumococci is the pore-forming toxin pneumolysin which stimulates cell death and is involved in the evasion of some defense mechanisms. The immune system, however, employs different inflammasomes to sense pneumolysin-induced pore formation, cellular membrane damage, and/or subsequent leakage of bacterial nucleic acid into the host cell cytosol. Canonical inflammasomes are cytosolic multiprotein complexes consisting of a receptor molecule such as NLRP3 or AIM2, the adapter ASC, and caspase-1. NLRP3 and AIM2 inflammasomes mediate cell death and production of important IL-1 family cytokines to recruit leukocytes and defend against S. pneumoniae. Here, we review recent evidence that highlights inflammasomes as critical sensors of S. pneumoniae-induced cellular perturbations, summarize their role in pneumococcal infections, and discuss potential evasion strategies of some emerging pneumococcal strains.

Keywords: Inflammasome; Innate immunity; Pneumonia; Streptococcus pneumoniae.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Immune Evasion*
  • Immunity, Innate*
  • Inflammasomes / genetics
  • Inflammasomes / immunology*
  • Pneumococcal Infections / immunology*
  • Pneumococcal Infections / microbiology
  • Streptococcus pneumoniae / genetics
  • Streptococcus pneumoniae / immunology*
  • Streptococcus pneumoniae / physiology


  • Inflammasomes