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Translocation and surface expression of lipidated serogroup B capsular Polysaccharide in Neisseria meningitidis

Yih-Ling Tzeng1, Anup K Datta, Cristy A Strole

  • 1Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30033, USA.

Infection and Immunity
|February 26, 2005
PubMed

Insights

Neisseria meningitidis serogroup B lipA and lipB genes are crucial for translocating and expressing lipidated capsule polymers on the bacterial surface. Mutations in these genes lead to intracellular polymer accumulation and increased susceptibility to human serum killing.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • The capsule of Neisseria meningitidis serogroup B, a (alpha2-->8)-linked polysialic acid, is anchored to the outer membrane via a 1,2-diacylglycerol moiety.
  • Previous studies in Escherichia coli K-12 suggested that lipA and lipB gene deletions resulted in intracellular accumulation of capsule polymers lacking phospholipid substitution.

Purpose of the Study:

  • To investigate the function of lipA and lipB genes in capsule expression within a Neisseria meningitidis background.
  • To define the location, sequence, and relationship of these genes to other bacterial capsule genes.

Main Methods:

  • Generation of specific mutations in lipA and lipB in the Neisseria meningitidis serogroup B strain NMB.
  • Analysis of gene location and transcription within the ctr operon.
  • Assessment of capsular polymer production, lipid modification, and serum sensitivity.
  • Immunogold electron microscopy and flow cytometry for visualizing polymer location.
  • Gas chromatography-mass spectroscopy for detailed lipid anchor analysis.

Main Results:

  • LipA and lipB genes are located at the 3' end of the ctr operon and likely transcribed independently.
  • Inactivation of lipA, lipB, or both did not alter total capsular polymer levels but resulted in intracellular accumulation of polymers.
  • Mutants lacking functional lipA or lipB were sensitive to normal human serum killing, similar to unencapsulated strains.
  • Purified capsular polymers from mutants remained lipidated with a 1,2-dipalmitoyl glycerol moiety, identical to wild-type.

Conclusions:

  • LipA and LipB are not responsible for the diacylglycerophosphatidic acid substitution of the meningococcal capsule.
  • These genes are essential for the proper translocation and surface expression of the lipidated capsule polymer in Neisseria meningitidis.
  • Defects in lipA and lipB compromise bacterial defense mechanisms, increasing susceptibility to host immune responses.

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