ArticleScientific reports2019
The redox metabolic pathways function to limit Anaplasma phagocytophilum infection and multiplication while preserving fitness in tick vector cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Cellular immune response of Amblyomma sculptum and Amblyomma americanum to entomopathogenic fungi: Implications for biological tick control.Medical and veterinary entomology · 2026Article
- mGem: A tale as old as blood-do tick-borne pathogens exploit arthropod antioxidant defenses?mBio · 2026Review
- Cardiovascular Complications of Anaplasmosis: A Case of Acute Pulmonary Embolism and Literature Review.Infectious disease reports · 2026Article
- RmTIL, a cysteine-rich protein as a putative microbiota modulator from Rhipicephalus microplus tick.Parasitology research · 2026Article
- Immune-mediated microbial interference governsiScience · 2026Article
- Insights into tick-pathogen interactions - a single cell RNA sequencing approach of transcriptional changes during ehrlichial infection.bioRxiv : the preprint server for biology · 2026Article
- Article
- Alteration of mitochondrial function in arthropods during arboviruses infection: a review of the literature.Frontiers in physiology · 2025Review
- High Crimean-Congo hemorrhagic fever incidence linked to greater genetic diversity and differentiation in Hyalomma marginatum populations in Türkiye.Parasites & vectors · 2024Article
- Bacterial reprogramming of tick metabolism impacts vector fitness and susceptibility to infection.Nature microbiology · 2024Article
- Evasion of host antioxidative response via disruption of NRF2 signaling in fatal Ehrlichia-induced liver injury.PLoS pathogens · 2023Article
- Article
- PERK-mediated antioxidant response is key for pathogen persistence in ticks.bioRxiv : the preprint server for biology · 2023Article
- Rickettsial pathogen inhibits tick cell death through tryptophan metabolite mediated activation of p38 MAP kinase.iScience · 2023Article
- Ambivalent Roles of Oxidative Stress in Triangular Relationships among Arthropod Vectors, Pathogens and Hosts.Antioxidants (Basel, Switzerland) · 2022Review
- Redox Imbalance and Its Metabolic Consequences in Tick-Borne Diseases.Frontiers in cellular and infection microbiology · 2022Review
- The genus Anaplasma: drawing back the curtain on tick-pathogen interactions.Pathogens and disease · 2021Review
- Comparative analysis ofHeliyon · 2021Article
- Rickettsial pathogen uses arthropod tryptophan pathway metabolites to evade reactive oxygen species in tick cells.Cellular microbiology · 2020Article
- Tick and Host Derived Compounds Detected in the Cement Complex Substance.Biomolecules · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aerobic organisms evolved conserved mechanisms controlling the generation of reactive oxygen species (ROS) to maintain redox homeostasis signaling and modulate signal transduction, gene expression and cellular functional responses under physiological conditions. The production of ROS by mitochondria is essential in the oxidative stress associated with different pathologies and in response to pathogen infection. Anaplasma phagocytophilum is an intracellular pathogen transmitted by Ixodes scapularis ticks and causing human granulocytic anaplasmosis. Bacteria multiply in vertebrate neutrophils and infect first tick midgut cells and subsequently hemocytes and salivary glands from where transmission occurs. Previous results demonstrated that A. phagocytophilum does not induce the production of ROS as part of its survival strategy in human neutrophils. However, little is known about the role of ROS during pathogen infection in ticks. In this study, the role of tick oxidative stress during A. phagocytophilum infection was characterized through the function of different pathways involved in ROS production. The results showed that tick cells increase mitochondrial ROS production to limit A. phagocytophilum infection, while pathogen inhibits alternative ROS production pathways and apoptosis to preserve cell fitness and facilitate infection. The inhibition of NADPH oxidase-mediated ROS production by pathogen infection appears to occur in both neutrophils and tick cells, thus supporting that A. phagocytophilum uses common mechanisms for infection of ticks and vertebrate hosts. However, differences in ROS response to A. phagocytophilum infection between human and tick cells may reflect host-specific cell tropism that evolved during pathogen life cycle.
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