Evidence map›Paper›PMID 24486057›Full record

ReviewSeminars in immunology2014

Divergent neuroendocrine responses to localized and systemic inflammation.

Mark K Lukewich, Richard C Rogers, Alan E Lomax

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Time-sensitive therapeutics.Critical care (London, England) · 2017
    Review
  6. Review
  7. 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

3 authors at 3 institutions in 2 countries.

Mark K LukewichDepartment of Biological Sciences, Brock University, St. Catharines, Ontario, Canada.
Richard C RogersLaboratory for Autonomic Neuroscience, Pennington Biomedical Research Center, Baton Rouge, LA, USA.
Alan E LomaxDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada; Department of Medicine, Queen's University, Kingston, Ontario, Canada. Electronic address: lomaxa@queensu.ca.
Brock University · CAPennington Biomedical Research Center · USQueen's University · CA

Funding

TNF, VAGAL TONE AND GASTRIC MOTILITYR01DK052142 · NIDDK · OHIO STATE UNIVERSITY · PI ROGERS, RICHARD C. · 1997 to 2013
$3.1M
Brainstem Esophageal-Gastric ReflexesR01DK056373 · NIDDK · OHIO STATE UNIVERSITY · PI ROGERS, RICHARD C. · 1999 to 2009
$2.1M
Glial-Neural Interactions in Autonomic ControlR01NS060664 · NINDS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI ROGERS, RICHARD C. · 2008 to 2012
$1.6M
NIDDK NIH HHS R01 DK052142NIDDK NIH HHS R01 DK056373NINDS NIH HHS R01 NS060664
6 · The paper itself

Abstract

The sympathetic nervous system (SNS) is part of an integrative network that functions to restore homeostasis following injury and infection. The SNS can provide negative feedback control over inflammation through the secretion of catecholamines from postganglionic sympathetic neurons and adrenal chromaffin cells (ACCs). Central autonomic structures receive information regarding the inflammatory status of the body and reflexively modulate SNS activity. However, inflammation and infection can also directly regulate SNS function by peripheral actions on postganglionic cells. The present review discusses how inflammation activates autonomic reflex pathways and compares the effect of localized and systemic inflammation on ACCs and postganglionic sympathetic neurons. Systemic inflammation significantly enhanced catecholamine secretion through an increase in Ca(2+) release from the endoplasmic reticulum. In contrast, acute and chronic GI inflammation reduced voltage-gated Ca(2+) current. Thus it appears that the mechanisms underlying the effects of peripheral and systemic inflammation neuroendocrine function converge on the modulation of intracellular Ca(2+) signaling.

Indexed as

AnimalsCalciumCalcium SignalingCatecholaminesChromaffin CellsCytokinesFeedback, PhysiologicalGene Expression RegulationHumansInflammationInflammatory Bowel DiseasesNeuronsSepsisSympathetic Nervous SystemCalciumCatecholaminesCytokinesExcitation secretion couplingInflammatory bowel diseaseNeuroimmunologySepsisSympathetic nervous system

Identifiers

PMID24486057
PMCPMC4128895
OpenAlexW2065970011

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.