Evidence map›Paper›PMID 32562372›Full record

ArticleCellular microbiology2020

Rickettsial pathogen uses arthropod tryptophan pathway metabolites to evade reactive oxygen species in tick cells.

Mustapha Dahmani, John F Anderson, Hameeda Sultana, Girish Neelakanta

Open access · greenAbstract read
In one paragraph

Article in Cellular microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Duplication of a conserved mitochondrial enzyme gene arms parasitoid wasps with venom cytotoxicity and oogenesis regulation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
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  11. Towards modelling tick-virus interactions using the weakly pathogenicFrontiers in cellular and infection microbiology · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Mustapha DahmaniDepartment of Biological Sciences, Old Dominion University, Norfolk, Virginia, USA.
John F AndersonDepartment of Entomology, Connecticut Agricultural Experiment Station, New Haven, Connecticut, USA.
Hameeda SultanaDepartment of Biological Sciences, Old Dominion University, Norfolk, Virginia, USA.ORCID 0000-0002-5682-3108
Girish NeelakantaDepartment of Biological Sciences, Old Dominion University, Norfolk, Virginia, USA.ORCID 0000-0001-8374-9604
Old Dominion University · USConnecticut Agricultural Experiment Station · USUniversity of Maryland, College Park · US

Funding

Anaplasma Phagocytophilum Modulate Tick Gene Expression for its Survival and Transmission from the Vector HostR01AI130116 · NIAID · UNIVERSITY OF TENNESSEE KNOXVILLE · PI Girish Neelakanta · 2017 to 2026
$3.0M
NIAID NIH HHS R01 AI130116
6 · The paper itself

Abstract

Reactive oxygen species (ROS) that are induced upon pathogen infection plays an important role in host defence. The rickettsial pathogen Anaplasma phagocytophilum, which is primarily transmitted by Ixodes scapularis ticks in the United States, has evolved many strategies to escape ROS and survive in mammalian cells. However, little is known on the role of ROS in A. phagocytophilum infection in ticks. Our results show that A. phagocytophilum and hemin induce activation of l-tryptophan pathway in tick cells. Xanthurenic acid (XA), a tryptophan metabolite, supports A. phagocytophilum growth in tick cells through inhibition of tryptophan dioxygenase (TDO) activity leading to reduced l-kynurenine levels that subsequently affects build-up of ROS. However, hemin supports A. phagocytophilum growth in tick cells by inducing TDO activity leading to increased l-kynurenine levels and ROS production. Our data reveal that XA and kynurenic acid (KA) chelate hemin. Furthermore, treatment of tick cells with 3-hydroxyl l-kynurenine limits A. phagocytophilum growth in tick cells. RNAi-mediated knockdown of kynurenine aminotransferase expression results in increased ROS production and reduced A. phagocytophilum burden in tick cells. Collectively, these results suggest that l-tryptophan pathway metabolites influence A. phagocytophilum survival by affecting build up of ROS levels in tick cells.

Indexed as

Anaplasma phagocytophilumAnimalsHeminHost-Pathogen InteractionsHydrolasesIxodesKynurenic AcidKynurenineNADPReactive Oxygen SpeciesRNA InterferenceTransaminasesTryptophanTryptophan OxygenaseUp-RegulationXanthurenates3-hydroxykynurenineHeminHydrolasesKynurenic AcidkynureninaseKynureninekynurenine-oxoglutarate transaminaseNADPReactive Oxygen SpeciesTransaminasesTryptophanTryptophan OxygenaseXanthurenatesxanthurenic acidAnaplasma phagocytophilumheminIxodes scapulariskynurenic acidreactive oxygen speciesRickettsiatryptophan metabolitesxanthurenic acid

Identifiers

PMID32562372
PMCPMC7483324
OpenAlexW3036169206

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.