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Development and Identification of a Novel Subpopulation of Human Neutrophil-derived Giant Phagocytes In Vitro
Published on: January 25, 2017
Defective phagocytosis in Anaplasma phagocytophilum-infected neutrophils
Justin W A Garyu1, Kyoung-seong Choi, Dennis J Grab
1Department of Pathology, Division of Medical Microbiology, The Johns Hopkins University School of Medicine, 720 Rutland Avenue, Ross 624, Baltimore, MD 21205, USA.
Abstract:
Anaplasma phagocytophilum infection induces functional neutrophil changes. Using both Candida albicans and fluorescent-aggregate phagocytosis assays, we examined whether neutrophil and dimethyl sulfoxide-differentiated HL-60 cell infection impairs internalization. A. phagocytophilum infection significantly decreased phagocytosis compared to that of controls (P < 0.05). This further impairment of neutrophil function may promote opportunistic infections and exacerbate disease.
Insights
Anaplasma phagocytophilum infection impairs neutrophil phagocytosis, a key immune defense mechanism. This reduced ability to engulf pathogens may increase the risk of secondary infections and worsen disease severity.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Neutrophils are critical immune cells for fighting infections.
- Anaplasma phagocytophilum is a bacterial pathogen known to infect neutrophils.
- Neutrophil dysfunction can lead to increased susceptibility to opportunistic infections.
Purpose of the Study:
- To investigate the impact of Anaplasma phagocytophilum infection on neutrophil phagocytic function.
- To determine if A. phagocytophilum infection impairs the ability of neutrophils and HL-60 cells to internalize pathogens.
Main Methods:
- Utilized Candida albicans phagocytosis assay.
- Employed fluorescent-aggregate phagocytosis assay.
- Infected neutrophils and dimethyl sulfoxide-differentiated HL-60 cells with A. phagocytophilum.
Main Results:
- A. phagocytophilum infection significantly reduced phagocytosis compared to control groups (P < 0.05).
- The impairment in phagocytosis was observed in both primary neutrophils and HL-60 cell models.
Conclusions:
- Anaplasma phagocytophilum infection compromises neutrophil phagocytic capacity.
- Impaired neutrophil function due to A. phagocytophilum may facilitate opportunistic infections.
- This functional deficit could contribute to disease exacerbation.
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