Evidence map›Paper›PMID 34174901›Full record

ArticleJournal of neuroinflammation2021

Beyond the lesion site: minocycline augments inflammation and anxiety-like behavior following SCI in rats through action on the gut microbiota.

Emma K A Schmidt, Pamela J F Raposo, Abel Torres-Espin, Keith K Fenrich, Karim Fouad

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 3 pooled it
5.0field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 3 syntheses or guidelines pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. 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

5 authors at 2 institutions in 2 countries.

Emma K A SchmidtNeuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada.
Pamela J F RaposoFaculty of Rehabilitation Medicine, University of Alberta, 3-48 Corbett Hall, Edmonton, Alberta, T6G 2G4, Canada.
Abel Torres-EspinDepartment of Neurological Surgery, University of California San Francisco, Brain and Spinal Injury Center, San Francisco, CA, USA.
Keith K FenrichNeuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada.
Karim FouadNeuroscience and Mental Health Institute, University of Alberta, Edmonton, Alberta, Canada. karim.fouad@ualberta.ca.ORCID http://orcid.org/0000-0003-3654-7852
University of Alberta · CAUniversity of California, San Francisco · US

Funding

Craig H. Neilsen Foundation NPRG 542589
6 · The paper itself

Abstract

backgroundMinocycline is a clinically available synthetic tetracycline derivative with anti-inflammatory and antibiotic properties. The majority of studies show that minocycline can reduce tissue damage and improve functional recovery following central nervous system injuries, mainly attributed to the drug's direct anti-inflammatory, anti-oxidative, and neuroprotective properties. Surprisingly the consequences of minocycline's antibiotic (i.e., antibacterial) effects on the gut microbiota and systemic immune response after spinal cord injury have largely been ignored despite their links to changes in mental health and immune suppression.

methodsHere, we sought to determine minocycline's effect on spinal cord injury-induced changes in the microbiota-immune axis using a cervical contusion injury in female Lewis rats. We investigated a group that received minocycline following spinal cord injury (immediately after injury for 7 days), an untreated spinal cord injury group, an untreated uninjured group, and an uninjured group that received minocycline. Plasma levels of cytokines/chemokines and fecal microbiota composition (using 16s rRNA sequencing) were monitored for 4 weeks following spinal cord injury as measures of the microbiota-immune axis. Additionally, motor recovery and anxiety-like behavior were assessed throughout the study, and microglial activation was analyzed immediately rostral to, caudal to, and at the lesion epicenter.

resultsWe found that minocycline had a profound acute effect on the microbiota diversity and composition, which was paralleled by the subsequent normalization of spinal cord injury-induced suppression of cytokines/chemokines. Importantly, gut dysbiosis following spinal cord injury has been linked to the development of anxiety-like behavior, which was also decreased by minocycline. Furthermore, although minocycline attenuated spinal cord injury-induced microglial activation, it did not affect the lesion size or promote measurable motor recovery.

conclusionWe show that minocycline's microbiota effects precede its long-term effects on systemic cytokines and chemokines following spinal cord injury. These results provide an exciting new target of minocycline as a therapeutic for central nervous system diseases and injuries.

Indexed as

AnimalsAnxietyCytokinesDisease Models, AnimalDysbiosisFemaleGastrointestinal MicrobiomeInflammationMicrogliaMinocyclineRatsRats, Inbred LewRecovery of FunctionSpinal Cord InjuriesCytokinesMinocyclineInflammationMicrobiotaMinocyclineSpinal cord injury

Identifiers

PMID34174901
PMCPMC8234629
OpenAlexW3173220324

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.