Anaplasma phagocytophilum infection induces apoptosis in HL-60 cells

Pratap Karki; Jacob W. IJdo

doi:10.1007/s11274-011-0745-z

Anaplasma phagocytophilum infection induces apoptosis in HL-60 cells

Pratap Karki, Jacob W. IJdo

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1 Scopus citations

Abstract

Anaplasma phagocytophilum, the causative agent of human granulocytic anaplasmosis, is an obligate intracellular bacterium that survives in neutrophils by delaying apoptosis. The human promyelocytic leukemia cell line HL-60 has been the ultimate choice for culturing Anaplasma in vitro. In this study, we assessed the various events of drug-induced apoptosis in A. phagocytophilum-infected HL-60 cells. Anaplasma infection reduced the cell viability and increased the apoptosis in HL-60 cells and staurosporine or etoposide-induced apoptosis was further exacerbated with Anaplasma infection. Altogether our results suggest that A. phagocytophilum infection is proapoptotic in HL-60 cells unlike in neutrophils where it is antiapoptotic.

Original language	English (US)
Pages (from-to)	2741-2746
Number of pages	6
Journal	World Journal of Microbiology and Biotechnology
Volume	27
Issue number	11
DOIs	https://doi.org/10.1007/s11274-011-0745-z
State	Published - Nov 2011
Externally published	Yes

Bibliographical note

Funding Information:
Acknowledgments This study was supported in part by a grant from National Institute of Health (RO1AI076244) to JWI. We would like to thank Mark Ver Meer and Elizabeth L. Kennedy for their helpful discussions.

Keywords

Anaplasma
Anaplasmosis
Apoptosis
HL-60
Neutrophils

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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title = "Anaplasma phagocytophilum infection induces apoptosis in HL-60 cells",

abstract = "Anaplasma phagocytophilum, the causative agent of human granulocytic anaplasmosis, is an obligate intracellular bacterium that survives in neutrophils by delaying apoptosis. The human promyelocytic leukemia cell line HL-60 has been the ultimate choice for culturing Anaplasma in vitro. In this study, we assessed the various events of drug-induced apoptosis in A. phagocytophilum-infected HL-60 cells. Anaplasma infection reduced the cell viability and increased the apoptosis in HL-60 cells and staurosporine or etoposide-induced apoptosis was further exacerbated with Anaplasma infection. Altogether our results suggest that A. phagocytophilum infection is proapoptotic in HL-60 cells unlike in neutrophils where it is antiapoptotic.",

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author = "Pratap Karki and IJdo, {Jacob W.}",

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AU - IJdo, Jacob W.

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N2 - Anaplasma phagocytophilum, the causative agent of human granulocytic anaplasmosis, is an obligate intracellular bacterium that survives in neutrophils by delaying apoptosis. The human promyelocytic leukemia cell line HL-60 has been the ultimate choice for culturing Anaplasma in vitro. In this study, we assessed the various events of drug-induced apoptosis in A. phagocytophilum-infected HL-60 cells. Anaplasma infection reduced the cell viability and increased the apoptosis in HL-60 cells and staurosporine or etoposide-induced apoptosis was further exacerbated with Anaplasma infection. Altogether our results suggest that A. phagocytophilum infection is proapoptotic in HL-60 cells unlike in neutrophils where it is antiapoptotic.

AB - Anaplasma phagocytophilum, the causative agent of human granulocytic anaplasmosis, is an obligate intracellular bacterium that survives in neutrophils by delaying apoptosis. The human promyelocytic leukemia cell line HL-60 has been the ultimate choice for culturing Anaplasma in vitro. In this study, we assessed the various events of drug-induced apoptosis in A. phagocytophilum-infected HL-60 cells. Anaplasma infection reduced the cell viability and increased the apoptosis in HL-60 cells and staurosporine or etoposide-induced apoptosis was further exacerbated with Anaplasma infection. Altogether our results suggest that A. phagocytophilum infection is proapoptotic in HL-60 cells unlike in neutrophils where it is antiapoptotic.

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KW - Neutrophils

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Anaplasma phagocytophilum infection induces apoptosis in HL-60 cells

Abstract

Bibliographical note

Keywords

UN SDGs

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