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Research Article Free access | 10.1172/JCI1544

The agent of Human Granulocytic Ehrlichiosis resides in an endosomal compartment.

P Webster, J W IJdo, L M Chicoine, and E Fikrig

Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06520-8031, USA.

Find articles by Webster, P. in: JCI | PubMed | Google Scholar

Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06520-8031, USA.

Find articles by IJdo, J. in: JCI | PubMed | Google Scholar

Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06520-8031, USA.

Find articles by Chicoine, L. in: JCI | PubMed | Google Scholar

Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06520-8031, USA.

Find articles by Fikrig, E. in: JCI | PubMed | Google Scholar

Published May 1, 1998 - More info

Published in Volume 101, Issue 9 on May 1, 1998
J Clin Invest. 1998;101(9):1932–1941. https://doi.org/10.1172/JCI1544.
© 1998 The American Society for Clinical Investigation
Published May 1, 1998 - Version history
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Abstract

The composition of cytoplasmic vacuoles containing the agent of Human Granulocytic Ehrlichiosis (HGE) was studied to investigate how this pathogen exists within infected host cells. Electron microscopy demonstrated that the HGE organism resides in a membrane-bound compartment within HL-60 cells: early forms of the HGE agent have a round reticular appearance while later structures are small and dense. Vacuoles containing HGE bacteria incorporated endocytosed colloidal gold particles, suggesting that they are part of the endocytic pathway. Antibodies directed to the mannose-6-phosphate receptor labeled vacuole membranes. Antibodies to the transferrin receptor and to the lysosomal membrane glycoprotein LAMP 1 did not. Moreover, 3-(2,4-dinitroanilino)-3'-amino-N-methyldipropylamine, which normally accumulates in compartments with low pH, was not present inside these vacuoles. These results suggest that vacuoles containing the agent of HGE fail to mature into phagolysosomes. We conclude that the agent of HGE appears to enter and modify part of the endocytic pathway.

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