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Entry and intracellular replication of Escherichia coli K1 in macrophages require expression of outer membrane

Sunil K Sukumaran1, Hiroyuki Shimada, Nemani V Prasadarao

  • 1Division of Infectious Diseases, Children's Hospital Los Angeles and Keck School of Medicine, University of Southern California, 4650 Sunset Boulevard, Los Angeles, CA 90027, USA.

Infection and Immunity
|September 23, 2003
PubMed

Insights

Escherichia coli K1 invades macrophages, surviving and replicating inside them. Outer membrane protein A (OmpA) enhances this interaction, facilitating bacterial entry and survival, which may contribute to meningitis development.

Area of Science:

  • Microbiology
  • Immunology
  • Neonatal Infectious Diseases

Background:

  • Escherichia coli K1 is a significant cause of neonatal meningitis.
  • The interaction between E. coli K1 and macrophages remains poorly understood.

Purpose of the Study:

  • To investigate the interaction between E. coli K1 and macrophages.
  • To determine the role of Outer membrane protein A (OmpA) in this interaction.

Main Methods:

  • In vitro studies using murine and human macrophage cell lines, monocytes, and macrophages from newborn rats.
  • Opsonization assays.
  • Transmission electron microscopy and immunocytochemistry.
  • Cellular process studies (actin and microtubule dependence).

Main Results:

  • E. coli K1 enters, survives, and replicates intracellularly in macrophages and monocytes.
  • OmpA expression on E. coli facilitates binding, phagocytosis, and intracellular survival.
  • Bacterial uptake and survival are independent of opsonization.
  • OmpA(+) E. coli replicates within a single phagosome, leading to cell lysis.
  • Internalization involves actin- and microtubule-dependent pathways, independent of RGD-mediated integrin receptors.

Conclusions:

  • Intracellular survival and replication of E. coli K1 within phagocytic cells are critical for bacteremia and subsequent blood-brain barrier crossing.
  • OmpA is a key virulence factor for E. coli K1 interaction with macrophages.

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