Evidence map›Paper›PMID 33385413›Full record

ArticleExperimental and molecular pathology2021

Effects of 9-t-butyl doxycycline on the innate immune response to CNS ischemia-reperfusion injury.

Nguyen Mai, Sara A Knowlden, Kathleen Miller-Rhodes, Viollandi Prifti, Max Sims, Mark Grier, Mark Nelson, Marc W Halterman

Open access · greenAbstract read
In one paragraph

Article in Experimental and molecular pathology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Network-based prediction and real-world patient data observation identify doxycycline as a repurposable drug in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  2. Article
  3. 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

8 authors at 3 institutions in 1 country.

Nguyen MaiDepartment of Neuroscience, University of Rochester Medical Center, Rochester, NY 14642, USA; The Center for Neurotherapeutics Discovery, University of Rochester Medical Center, Rochester, NY 14642, USA.
Sara A KnowldenDepartment of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA; The Center for Neurotherapeutics Discovery, University of Rochester Medical Center, Rochester, NY 14642, USA.
Kathleen Miller-RhodesDepartment of Neuroscience, University of Rochester Medical Center, Rochester, NY 14642, USA; The Center for Neurotherapeutics Discovery, University of Rochester Medical Center, Rochester, NY 14642, USA.
Viollandi PriftiDepartment of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA; The Center for Neurotherapeutics Discovery, University of Rochester Medical Center, Rochester, NY 14642, USA.
Max SimsDepartment of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA; The Center for Neurotherapeutics Discovery, University of Rochester Medical Center, Rochester, NY 14642, USA.
Mark GrierEchelon Biosciences, Salt Lake City, UT 84108, USA.
Mark NelsonEchelon Biosciences, Salt Lake City, UT 84108, USA.
Marc W HaltermanDepartment of Neurology, SUNY Stony Brook, Stony Brook, NY, USA. Electronic address: marc.halterman@stonybrookmedicine.edu.
University of Rochester Medical Center · USEchelon Biosciences · USStony Brook University · US

Funding

Mechanisms of lung-dependent neutrophil priming in global cerebral ischemia-reperfusion injuryR01NS092455 · NINDS · UNIVERSITY OF ROCHESTER · PI HALTERMAN, MARC W · 2015 to 2025
$4.5M
Role of lung-brain coupling on neutrophil priming and reperfusion injury following global cerebral ischemiaF30NS092168 · NINDS · UNIVERSITY OF ROCHESTER · PI MAI, NGUYEN · 2015 to 2018
$195k
NINDS NIH HHS F30 NS092168NINDS NIH HHS R01 NS092455
6 · The paper itself

Abstract

Cerebral ischemia triggers a cascade of neuroinflammatory and peripheral immune responses that contribute to post-ischemic reperfusion injury. Prior work conducted in CNS ischemia models underscore the potential to harness non-antibiotic properties of tetracycline antibiotics for therapeutic benefit. In the present study, we explored the immunomodulatory effects of the tetracycline derivative 9-tert-butyl doxycycline (9-TB) in a mouse model of transient global ischemia that mimics immunologic aspects of the post-cardiac arrest syndrome. Pharmacokinetic studies performed in C57BL/6 mice demonstrate that within four hours after delivery, levels of 9-TB in the brain were 1.6 and 9.5-fold higher than those obtained using minocycline and doxycycline, respectively. Minocycline and 9-TB also dampened inflammation, measured by reduced TNFα-inducible, NF-κβ-dependent luciferase activity in a microglial reporter line. Notably, daily 9-TB treatment following ischemia-reperfusion injury in vivo induced the retention of polymorphonuclear neutrophils (PMNs) within the spleen while simultaneously biasing CNS PMNs towards an anti-inflammatory (CD11b

Indexed as

AnimalsAnti-Bacterial AgentsAnti-Inflammatory AgentsBlood-Brain BarrierBrain IschemiaDisease Models, AnimalDoxycyclineImmunity, InnateInflammationMaleMiceMice, Inbred C57BLMyeloid CellsReperfusion InjuryAnti-Bacterial AgentsAnti-Inflammatory AgentsDoxycyclineCerebral ischemiaInnate immunityNeuroinflammationNeutrophilTetracycline

Identifiers

PMID33385413
PMCPMC9139467
OpenAlexW3115797140

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.