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Listeria intracellular growth and virulence require host-derived lipoic acid

Mary O'Riordan1, Marlena A Moors, Daniel A Portnoy

  • 1Department of Molecular and Cell Biology, School of Public Health, University of California, Berkeley, CA 94720-3202, USA. oriordan@umich.edu

Science (New York, N.Y.)
|October 18, 2003
PubMed

Insights

Listeria monocytogenes requires the lipoate protein ligase LplA1 for growth within host cells. This enzyme is crucial for pathogen virulence, as its absence significantly reduces bacterial survival and infectivity in animal models.

Area of Science:

  • Microbiology
  • Pathogen Biology
  • Molecular Biology

Background:

  • Listeria monocytogenes is a significant intracellular pathogen.
  • It causes severe illness in vulnerable populations, including pregnant women and immunocompromised individuals.

Purpose of the Study:

  • To investigate the role of lipoate protein ligase LplA1 in L. monocytogenes pathogenesis.
  • To understand the mechanism by which LplA1 contributes to bacterial growth and virulence within the host.

Main Methods:

  • Genetic manipulation of L. monocytogenes to create a strain lacking LplA1 (DeltalplA1).
  • Assessment of bacterial growth in host cell cytosol.
  • Evaluation of bacterial virulence in animal models.

Main Results:

  • The DeltalplA1 strain exhibited defective growth specifically within the host cytosol.
  • Virulence was reduced by a factor of 300 in animal models compared to the wild-type strain.
  • Loss of lipoylation on the E2 subunit of pyruvate dehydrogenase (PDH) was observed in the DeltalplA1 strain during intracellular growth, indicating impaired PDH function.

Conclusions:

  • LplA1 is essential for L. monocytogenes growth and virulence in vivo.
  • Impaired pyruvate dehydrogenase function due to lack of lipoylation is a key factor in the reduced virulence of the DeltalplA1 strain.
  • Bacterial utilization of host-derived lipoic acid is critical for intracellular replication of pathogens.

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