Evidence map›Paper›PMID 24929192›Full record

ArticleBrain, behavior, and immunity2014

Kinetic characteristics of euflammation: the induction of controlled inflammation without overt sickness behavior.

Andrew J Tarr, Xiaoyu Liu, Nathaniel S Reed, Ning Quan

Abstract read
In one paragraph

Article in Brain, behavior, and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Review
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  11. Review
  12. Article
  13. Review
  14. Neuroinflammation: the devil is in the details.Journal of neurochemistry · 2016
    Review
  15. Article
  16. 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.

Andrew J TarrDivision of Biosciences, The Ohio State University, 305 W. 12th Ave, Columbus, OH 43210, USA; Institute for Behavioral Medicine Research, The Ohio State University Wexner Medical Center, 460 Medical Center Dr., Columbus, OH 43210, USA. Electronic address: andrew.tarr@osumc.edu.
Xiaoyu LiuDivision of Biosciences, The Ohio State University, 305 W. 12th Ave, Columbus, OH 43210, USA; Institute for Behavioral Medicine Research, The Ohio State University Wexner Medical Center, 460 Medical Center Dr., Columbus, OH 43210, USA.
Nathaniel S ReedDivision of Biosciences, The Ohio State University, 305 W. 12th Ave, Columbus, OH 43210, USA; Institute for Behavioral Medicine Research, The Ohio State University Wexner Medical Center, 460 Medical Center Dr., Columbus, OH 43210, USA.
Ning QuanDivision of Biosciences, The Ohio State University, 305 W. 12th Ave, Columbus, OH 43210, USA; Institute for Behavioral Medicine Research, The Ohio State University Wexner Medical Center, 460 Medical Center Dr., Columbus, OH 43210, USA. Electronic address: quan.14@osu.edu.

Funding

IL-1R1 promoter complex in the neuroendocrine, nervous, and immune systemsR01AI076926 · NIAID · OHIO STATE UNIVERSITY · PI QUAN, NING · 2008 to 2012
$1.9M
NIAID NIH HHS R01 AI076926NIAID NIH HHS R01AI-076926
6 · The paper itself

Abstract

We found recently that controlled progressive challenge with subthreshold levels of E. coli can confer progressively stronger resistance to future reinfection-induced sickness behavior to the host. We have termed this type of inflammation "euflammation". In this study, we further characterized the kinetic changes in the behavior, immunological, and neuroendocrine aspects of euflammation. Results show euflammatory animals only display transient and subtle sickness behaviors of anorexia, adipsia, and anhedonia upon a later infectious challenge which would have caused much more severe and longer lasting sickness behavior if given without prior euflammatory challenges. Similarly, infectious challenge-induced corticosterone secretion was greatly ameliorated in euflammatory animals. At the site of E.coli priming injections, which we termed euflammation induction locus (EIL), innate immune cells displayed a partial endotoxin tolerant phenotype with reduced expression of innate activation markers and muted inflammatory cytokine expression upon ex vivo LPS stimulation, whereas innate immune cells outside EIL displayed largely opposite characteristics. Bacterial clearance function, however, was enhanced both inside and outside EIL. Finally, sickness induction by an infectious challenge placed outside the EIL was also abrogated. These results suggest euflammation could be used as an efficient method to "train" the innate immune system to resist the consequences of future infectious/inflammatory challenges.

Indexed as

Illness BehaviorAnimalsBehavior, AnimalCorticosteroneEscherichia coliInflammationMacrophages, PeritonealMaleMiceMotor ActivityPhagocytosisSpleenCorticosteroneE. coliEuflammationInflammationInnate immunityNeural-immuneSickness behavior

Identifiers

PMID24929192
PMCPMC4254289

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Registered trials

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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.