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Intratracheal Inoculation of Fischer 344 Rats with Francisella tularensis
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Francisella tularensis Confronts the Complement System.

Susan R Brock1, Michael J Parmely1

  • 1Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, Kansas City, KS, United States.

Frontiers in Cellular and Infection Microbiology
|January 10, 2018
PubMed
Summary

Francisella tularensis evades immune defenses by manipulating the complement system. Complement C3 opsonization enhances bacterial uptake but also triggers host cell death, revealing new insights into tularemia pathogenesis.

Keywords:
C3Francisella tularensiscell deathcomplementmacrophage

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Area of Science:

  • Immunology
  • Microbiology
  • Pathogenesis

Background:

  • Francisella tularensis employs immune evasion strategies, notably interacting with the complement system.
  • The bacterium's cell wall resists complement-mediated lysis, conferring serum resistance.
  • Complement C3 opsonization enhances F. tularensis uptake by immune cells like macrophages.

Purpose of the Study:

  • To investigate the role of complement C3 in F. tularensis pathogenesis and host cell interactions.
  • To explore the proposed C3 sensing system in human macrophages responding to intracellular C3b.
  • To elucidate how F. tularensis utilizes complement C3 for immune evasion and host cell manipulation.

Main Methods:

  • Exposure of F. tularensis to fresh human serum to study complement activation and opsonization.
  • Analysis of bacterial uptake by human neutrophils, dendritic cells, and macrophages.
  • Investigating the role of Complement Receptor 3 in F. tularensis opsonophagocytosis.
  • Assessing the impact of C3 opsonization on infected human macrophage survival and death.

Main Results:

  • Complement activation leads to C3b and iC3b deposition on F. tularensis, enhancing its uptake by immune cells.
  • Complement Receptor 3 plays a role in F. tularensis uptake by macrophages, potentially antagonizing TLR2 signaling.
  • C3 opsonization of F. tularensis SCHU S4 significantly increases infected macrophage death, independent of pathogen replication.
  • Intracellular C3 peptides, following phagosome escape, are proposed to act as danger signals triggering host cell death.

Conclusions:

  • Francisella tularensis effectively manipulates the complement system for immune evasion and enhanced host cell entry.
  • Complement C3 opsonization, while promoting uptake, paradoxically leads to host macrophage death.
  • The proposed intracellular C3 sensing mechanism offers a novel perspective on tularemia pathogenesis.
  • Further research into intracellular C3 roles may significantly advance our understanding of tularemia.