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A surface lipoprotein on Pasteurella multocida binds complement factor I to promote immune evasion.

Quynh Huong Nguyen1, Chun Heng Royce Lai1, Michael J Norris1

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Pasteurella multocida evades immune defenses by using its surface lipoprotein (PmSLP) to disable complement factor I (FI). This bacterial protein directly activates FI, blocking a key part of the immune system in cattle and humans.

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Area of Science:

  • Bacteriology
  • Immunology
  • Structural Biology

Background:

  • Pasteurella multocida is a significant pathogen causing wound infections in humans and severe diseases in cattle.
  • A subunit vaccine using the surface lipoprotein PmSLP has shown promise for cattle protection.
  • Understanding bacterial immune evasion mechanisms is crucial for developing effective treatments and vaccines.

Purpose of the Study:

  • To investigate the mechanism by which Pasteurella multocida evades the host immune system.
  • To elucidate the interaction between the bacterial surface lipoprotein PmSLP and host complement factor I (FI).
  • To determine the structural basis for PmSLP-mediated complement evasion.

Main Methods:

  • Biochemical assays to study the interaction between PmSLP and complement factor I (FI).
  • Complement component cleavage assays to assess FI activity.
  • Cryo-electron microscopy (Cryo-EM) to determine the structure of PmSLP bound to FI.

Main Results:

  • The Pasteurella multocida surface lipoprotein PmSLP directly binds and activates host complement factor I (FI).
  • PmSLP facilitates the cleavage of complement components C3b and C4b independently of cofactors, thereby inhibiting complement activation.
  • The cryo-EM structure reveals PmSLP stabilizes the catalytic domain of FI, enhancing its enzymatic activity.
  • This represents the first identified bacterial protein that directly activates FI, targeting all complement pathways.

Conclusions:

  • Pasteurella multocida employs a novel immune evasion strategy by hijacking complement factor I through its surface lipoprotein PmSLP.
  • This mechanism allows the bacterium to evade the complement system, a critical component of innate immunity.
  • The findings provide insights into pathogen-host interactions and potential targets for therapeutic interventions against Pasteurella multocida infections.