Related Experiment Video
Updated: May 28, 2026

LPS and ATP-induced Death of PMA-differentiated THP-1 Macrophages and its Validation
Published on: May 3, 2024
Anaplasma phagocytophilum infection induces apoptosis in HL-60 cells
1Inflammation Program and Division of Rheumatology, Department of Internal Medicine, University of Iowa and Veterans Administration Medical Center, 2501 Crosspark Road, MTF E104, Coralville, Iowa City, IA 52241, USA.
Abstract:
Anaplasma phagocytophilum, the causative agent of human granulocytic anaplasmosis, is an obligate intra-cellular 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.
Insights
Anaplasma phagocytophilum infection promotes apoptosis in human leukemia cells (HL-60), unlike its anti-apoptotic effect in neutrophils. This finding impacts understanding of anaplasmosis pathogenesis.
Area of Science:
- Microbiology
- Cell Biology
- Pathogenesis
Background:
- Anaplasma phagocytophilum causes human granulocytic anaplasmosis.
- This obligate intracellular bacterium delays neutrophil apoptosis for survival.
- The HL-60 cell line is commonly used for in vitro Anaplasma culture.
Purpose of the Study:
- To investigate the effects of Anaplasma phagocytophilum infection on drug-induced apoptosis in HL-60 cells.
- To compare the apoptotic response in infected HL-60 cells versus neutrophils.
Main Methods:
- Culturing Anaplasma phagocytophilum in HL-60 cells.
- Inducing apoptosis using staurosporine and etoposide.
- Assessing cell viability and apoptosis markers.
Main Results:
- Anaplasma infection reduced HL-60 cell viability.
- Infection increased spontaneous and drug-induced apoptosis in HL-60 cells.
- Apoptosis was significantly exacerbated by Anaplasma in staurosporine/etoposide-treated cells.
Conclusions:
- Anaplasma phagocytophilum infection exhibits a pro-apoptotic effect in HL-60 cells.
- This contrasts with the known anti-apoptotic role of the bacterium in neutrophils.
- Findings suggest differential apoptotic regulation by Anaplasma in distinct host cell types.
Related Concept Videos
Phagocytosis of Apoptotic Cells
Normal cells contain receptors that prevent them from being recognized by phagocytes.
Cells of the Innate Immune Response
Phagocytes
Phagocytes police the peripheral tissues by removing cellular debris and responding to the invasion of foreign substances or pathogens. Many phagocytes attack and remove microorganisms even before lymphocytes detect them. The human body has two general...
Immune Surveillance by NK Cells and Phagocytes
Natural Killer Cells: The Fast Responders
NK cells are large granular lymphocytes found in the blood and lymphatic system. These...
The Intrinsic Apoptotic Pathway
Autophagic Cell Death
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Apoptosis

