ArticleInfection and immunity2004
Anaplasma phagocytophilum utilizes multiple host evasion mechanisms to thwart NADPH oxidase-mediated killing during neutrophil infection.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
68 citing papers in PubMed.
- mGem: A tale as old as blood-do tick-borne pathogens exploit arthropod antioxidant defenses?mBio · 2026Review
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- An arthropod transporter IsOATP4056 exerts inhibitory effect on its interacting membrane protein to facilitate rickettsial pathogen survival in ticks.Cell communication and signaling : CCS · 2025Article
- Genetic resistance to vector-borne hemoprotozoa in livestock: molecular markers, host-parasite interactions, and implications for breeding and control.Journal of veterinary science · 2025Review
- Arthropod autophagy molecules facilitate Anaplasma phagocytophilum infection of Ixodes scapularis tick cells.Communications biology · 2025Article
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- Temporal patterns of gene expression in response to inoculation with a virulent Anaplasma phagocytophilum strain in sheep.Scientific reports · 2023Article
- Article
- Development of a Syndromic Molecular Diagnostic Assay for Tick-Borne Pathogens Using Barcoded Magnetic Bead Technology.Microbiology spectrum · 2023Article
- PERK-mediated antioxidant response is key for pathogen persistence in ticks.bioRxiv : the preprint server for biology · 2023Article
- Autophagy in protists and their hosts: When, how and why?Autophagy reports · 2023Article
- Vaccination with Mycoplasma pneumoniae membrane lipoproteins induces IL-17A driven neutrophilia that mediates Vaccine-Enhanced Disease.NPJ vaccines · 2022Article
- Article
- Disruption of VirB6 Paralogs in Anaplasma phagocytophilum Attenuates Its Growth.Journal of bacteriology · 2020Article
- Article
- Global Transcription Profiles ofFrontiers in veterinary science · 2020Article
- Neutrophils in innate immunity and systems biology-level approaches.Wiley interdisciplinary reviews. Systems biology and medicine · 2020Article
- Ixodes scapularis Src tyrosine kinase facilitates Anaplasma phagocytophilum survival in its arthropod vector.Ticks and tick-borne diseases · 2019Article
- The roles of NADPH oxidase in modulating neutrophil effector responses.Molecular oral microbiology · 2019Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Anaplasma phagocytophilum, the etiologic agent of human anaplasmosis, is a bacterial pathogen that specifically colonizes neutrophils. Neutrophils utilize the NADPH oxidase complex to generate superoxide (O(2)(-)) and initiate oxidative killing of microorganisms. A. phagocytophilum's unique tropism for neutrophils, however, indicates that it subverts and/or avoids oxidative killing. We therefore examined the effects of A. phagocytophilum infection on neutrophil NADPH oxidase assembly and reactive oxygen species (ROS) production. Following neutrophil binding, Anaplasma invasion requires at least 240 min. During its prolonged association with the neutrophil plasma membrane, A. phagocytophilum stimulates NADPH oxidase assembly, as indicated by increased cytochrome b(558) mobilization to the membrane, as well as colocalization of Rac and p22(phox). This initial stimulation taxes the host neutrophil's finite oxidase reserves, as demonstrated by time- and bacterial-dose-dependent decreases in secondary activation by N-formyl-methionyl-leucyl-phenylalanine (FMLP) or phorbol myristate acetate (PMA). This stimulation is modest, however, and does not diminish oxidase stores to nearly the extent that Escherichia coli, serum-opsonized zymosan, FMLP, or PMA do. Despite the apparent activation of NADPH oxidase, no change in ROS-dependent chemiluminescence is observed upon the addition of A. phagocytophilum to neutrophils, indicating that the bacterium may scavenge exogenous O(2)(-). Indeed, A. phagocytophilum rapidly detoxifies O(2)(-) in a cell-free system. Once internalized, the bacterium resides within a protective vacuole that excludes p22(phox) and gp91(phox). Thus, A. phagocytophilum employs at least two strategies to protect itself from neutrophil NADPH oxidase-mediated killing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.