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NalP-mediated proteolytic release of lactoferrin-binding protein B from the meningococcal cell surface

Virginie Roussel-Jazédé1, Ilse Jongerius, Martine P Bos

  • 1Department of Molecular Microbiology, Institute of Biomembranes, Utrecht University, Utrecht, Netherlands.

Infection and Immunity
|April 28, 2010
PubMed

Insights

Neisseria meningitidis releases the immunogenic lactoferrin-binding protein B (LbpB) via NalP protease. This bacterial immune evasion strategy reduces antibody-mediated killing, aiding survival in human hosts.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Immunology

Background:

  • Neisseria meningitidis requires iron for growth and utilizes lactoferrin-binding proteins A (LbpA) and LbpB for iron acquisition from lactoferrin.
  • LbpA is an outer membrane iron transporter, and LbpB is a cell surface-exposed lipoprotein.

Purpose of the Study:

  • To investigate the release of LbpB into the culture medium by Neisseria meningitidis.
  • To identify the protease responsible for LbpB release.
  • To determine the impact of LbpB release on bacterial survival against immune responses.

Main Methods:

  • Culturing Neisseria meningitidis under iron-limiting conditions.
  • Identifying the protease involved in LbpB release using genetic and biochemical approaches.
  • Assessing bacterial survival and complement-mediated killing in the presence of LbpB-specific antiserum.

Main Results:

  • LbpB was found to be released into the culture medium.
  • NalP, an autotransporter protease, was identified as responsible for LbpB release.
  • Release of LbpB decreased complement-mediated killing when bacteria were exposed to LbpB-specific antibodies.

Conclusions:

  • Neisseria meningitidis employs NalP to release LbpB, a secreted immunogenic protein.
  • This release mechanism represents a novel immune evasion strategy for N. meningitidis.
  • LbpB shedding may allow bacteria to evade antibody-dependent immune responses, facilitating colonization and persistence.

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