Breaking in and grabbing a meal: Anaplasma phagocytophilum cellular invasion, nutrient acquisition, and promising tools for their study

Hilary K. Truchan; David Seidman; Jason A. Carlyon

doi:10.1016/j.micinf.2013.10.010

Breaking in and grabbing a meal: Anaplasma phagocytophilum cellular invasion, nutrient acquisition, and promising tools for their study

Hilary K. Truchan, David Seidman, Jason A. Carlyon^*

^*Corresponding author for this work

Molecular Biosciences

Research output: Contribution to journal › Article › peer-review

34 Scopus citations

Abstract

Anaplasma phagocytophilum invades neutrophils to cause the emerging infection, human granulocytic anaplasmosis. Here, we provide a focused review of the A. phagocytophilum invasin-host cell receptor interactions that promote bacterial entry and the degradative and membrane traffic pathways that the organism exploits to route nutrients to the organelle in which it resides. Because its obligatory intracellular nature hinders knock out-complementation approaches, we also discuss the current methods used to study A. phagocytophilum gene function and the potential benefit of applying novel tools that have advanced studies of other obligate intracellular bacterial pathogens.

Original language	English (US)
Pages (from-to)	1017-1025
Number of pages	9
Journal	Microbes and Infection
Volume	15
Issue number	14-15
DOIs	https://doi.org/10.1016/j.micinf.2013.10.010
State	Published - Dec 2013

Funding

We apologize to our colleagues whose papers we could not cite due to space limitation. This work was supported by funding from NIH/NIAID grant 2R56 AI067283 . Scanning electron microscopy was performed in the VCU Department of Anatomy and Neurobiology Microscopy Facility, supported, in part, with funding from NIH-NINDS Center core grant 5P30NS047463 .

Keywords

Bacterial invasion
Ehrlichia
Nutritional virulence
Obligate intracellular
Rab GTPase
Rickettsia

ASJC Scopus subject areas

Microbiology
Immunology
Infectious Diseases

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10.1016/j.micinf.2013.10.010

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title = "Breaking in and grabbing a meal: Anaplasma phagocytophilum cellular invasion, nutrient acquisition, and promising tools for their study",

abstract = "Anaplasma phagocytophilum invades neutrophils to cause the emerging infection, human granulocytic anaplasmosis. Here, we provide a focused review of the A. phagocytophilum invasin-host cell receptor interactions that promote bacterial entry and the degradative and membrane traffic pathways that the organism exploits to route nutrients to the organelle in which it resides. Because its obligatory intracellular nature hinders knock out-complementation approaches, we also discuss the current methods used to study A. phagocytophilum gene function and the potential benefit of applying novel tools that have advanced studies of other obligate intracellular bacterial pathogens.",

keywords = "Bacterial invasion, Ehrlichia, Nutritional virulence, Obligate intracellular, Rab GTPase, Rickettsia",

author = "Truchan, {Hilary K.} and David Seidman and Carlyon, {Jason A.}",

note = "Funding Information: We apologize to our colleagues whose papers we could not cite due to space limitation. This work was supported by funding from NIH/NIAID grant 2R56 AI067283 . Scanning electron microscopy was performed in the VCU Department of Anatomy and Neurobiology Microscopy Facility, supported, in part, with funding from NIH-NINDS Center core grant 5P30NS047463 .",

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AU - Seidman, David

AU - Carlyon, Jason A.

N1 - Funding Information: We apologize to our colleagues whose papers we could not cite due to space limitation. This work was supported by funding from NIH/NIAID grant 2R56 AI067283 . Scanning electron microscopy was performed in the VCU Department of Anatomy and Neurobiology Microscopy Facility, supported, in part, with funding from NIH-NINDS Center core grant 5P30NS047463 .

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KW - Rab GTPase

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Breaking in and grabbing a meal: Anaplasma phagocytophilum cellular invasion, nutrient acquisition, and promising tools for their study

Abstract

Funding

Keywords

ASJC Scopus subject areas

Access to Document

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