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Pneumococcal pathogenesis: "innate invasion" yet organ-specific damage

Justin A Thornton1, Kelly Durick-Eder, Elaine I Tuomanen

  • 1Department of Infectious Diseases, St. Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN, 38105, USA.

Journal of Molecular Medicine (Berlin, Germany)
|February 18, 2010
PubMed

Insights

Streptococcus pneumoniae uses shared "innate invasion" mechanisms for pathogenesis, but organ-specific immune responses complicate protection strategies against infection and damage.

Area of Science:

  • Microbiology
  • Immunology
  • Pathogenesis

Background:

  • Streptococcus pneumoniae causes diverse infections, from nasopharyngeal colonization to invasive diseases.
  • Pathogen invasion mechanisms may involve conserved ligand/receptor interactions common to respiratory pathogens.
  • The innate immune response can target these invasion pathways.

Purpose of the Study:

  • To review the concept of an
  • innate invasion
  • mechanism in bacterial pathogenesis.

Main Methods:

  • Literature review of Streptococcus pneumoniae pathogenesis.
  • Analysis of host-pathogen interactions and immune responses.
  • Examination of organ-specific outcomes following infection.

Main Results:

  • Evidence suggests a primitive
  • innate invasion
  • mechanism underlies pathogenesis, shared by multiple respiratory pathogens.
  • The innate immune system possesses mechanisms to interrupt this invasion.
  • Organ responses to innate invasion activation vary significantly, impacting tissue damage.

Conclusions:

  • The concept of
  • innate invasion
  • provides a unifying framework for understanding pathogen progression.
  • Organ-specific immune responses present challenges for developing universal protective strategies.
  • Targeting innate invasion pathways requires consideration of differential organ susceptibility to damage.

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