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Intracellular parasitism by the human granulocytic ehrlichiosis bacterium through the P-selectin ligand, PSGL-1

M J Herron1, C M Nelson, J Larson

  • 1Division of Infectious Diseases, Department of Medicine, University of Minnesota School of Medicine, Minneapolis, MN 55455, USA.

Science (New York, N.Y.)
|June 2, 2000
PubMed

Insights

Human granulocytic ehrlichiosis (HGE) bacteria target neutrophils by binding to a specific molecule called PSGL-1. This interaction is crucial for HGE infection, highlighting a potential therapeutic target.

Area of Science:

  • Microbiology
  • Immunology
  • Cell Biology

Background:

  • Human granulocytic ehrlichiosis (HGE) is a febrile, tick-borne illness caused by an intracellular bacterium.
  • The HGE bacterium exhibits a specific tropism for phagocytic neutrophils.

Purpose of the Study:

  • To elucidate the molecular mechanism by which the HGE bacterium binds to and infects neutrophils.
  • To identify the specific host cell receptor involved in HGE pathogenesis.

Main Methods:

  • Utilized monoclonal antibodies targeting the P-selectin binding domain of leukocyte P-selectin glycoprotein ligand (PSGL-1).
  • Employed enzymatic digestion of PSGL-1 to assess its role in HGE binding.
  • Transfected nonsusceptible cells with complementary DNAs for PSGL-1 and alpha-(1,3) fucosyltransferase (Fuc-TVII) to evaluate HGE infectivity.

Main Results:

  • Monoclonal antibodies against PSGL-1 and enzymatic digestion of PSGL-1 inhibited HGE cell binding and infection.
  • Neoexpression of PSGL-1 and Fuc-TVII in nonsusceptible cells conferred susceptibility to HGE binding and infection.
  • Demonstrated that the HGE bacterium specifically binds to fucosylated PSGL-1 on leukocytes.

Conclusions:

  • The HGE bacterium utilizes fucosylated leukocyte PSGL-1 as its specific receptor for neutrophil targeting and infection.
  • Selectin mimicry is a key mechanism enabling the HGE bacterium's unique tropism for neutrophils.

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