Evidence map›Paper›PMID 23543756›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2013

Noradrenergic neurons regulate monocyte trafficking and mortality during gram-negative peritonitis in mice.

Eric J Seeley, Sophia S Barry, Saisindhu Narala, Michael A Matthay, Paul J Wolters

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

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  14. An overview of the role of sympathetic regulation of immune responses in infectious disease and autoimmunity.International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group · 2018
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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 1 country.

Eric J SeeleyDivision of Pulmonary, Critical Care, and Sleep Medicine, University of California, San Francisco, San Francisco, CA 94143, USA. eric.seeley@ucsf.edu
Sophia S Barry
Saisindhu Narala
Michael A Matthay
Paul J Wolters
University of California System · USUniversity of California, San Francisco · US

Funding

Sulfs and Injury Repair in Mucosal EpitheliaP01AI053194 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MOSTOV, KEITH E · 2002 to 2012
$13.4M
MECHANISMS OF ALVEOLAR EPITHELIAL FLUID CLEARANCER01HL051854 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTHAY, MICHAEL A. · 1994 to 2012
$4.4M
Resolution of Clinical Lung InjuryR37HL051856 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MATTHAY, MICHAEL A. · 2006 to 2015
$3.9M
RESOLUTION OF CLINICAL LUNG INJURYR01HL051856 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI MATTHAY, MICHAEL A. · 1996 to 2005
$1.7M
Mast Cells and the Host Response in the LungR01HL075026 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WOLTERS, PAUL J · 2004 to 2007
$1.5M
Regulation of Innate Immunity by the Sympathetic Nervous System Druing SepsisK08HL111202 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SEELEY, ERIC J. · 2012 to 2013
$263k
NHLBI NIH HHS HL-051854NHLBI NIH HHS HL-051856NHLBI NIH HHS HL075026NHLBI NIH HHS HL1112092-01A1NHLBI NIH HHS K08 HL111202NHLBI NIH HHS R01 HL051854NHLBI NIH HHS R01 HL051856NHLBI NIH HHS R01 HL075026NHLBI NIH HHS R37 HL051856NIAID NIH HHS AI-053194NIAID NIH HHS P01 AI053194
6 · The paper itself

Abstract

Effective host defense requires a robust, yet self-limited response to pathogens. A poorly calibrated response can lead to either bacterial dissemination due to insufficient inflammation or organ injury due to excessive inflammation. Recent evidence suggests that the cholinergic anti-inflammatory reflex helps calibrate the immune response. However, the influence of peripheral noradrenergic neurons, which are primarily sympathetic neurons, in regulating immunity remains incompletely characterized. Using a model of 6-hydroxydopamine-mediated noradrenergic nerve ablation, we show that elimination of noradrenergic neurons improves survival during Klebsiella pneumoniae peritonitis (67 versus 23%, p < 0.005) in mice. The survival benefit results from enhanced MCP-1-dependent monocyte recruitment and a subsequent decrease in bacterial loads. Splenectomy eliminated both the survival benefit of 6-hydroxydopamine and monocyte recruitment, suggesting that monocytes recruited to the peritoneum originate in the spleen. These results suggest that noradrenergic neurons regulate the immune response through two pathways. First, sympathetic nerve-derived norepinephrine directly restrains MCP-1 production by peritoneal macrophages during infection. Second, norepinephrine derived from the vagally innervated splenic nerve regulates splenic monocyte egress. Removal of these two modulators of the immune response enhances antibacterial immunity and improves survival. These results may have implications for how states of catecholamine excess influence the host response to bacterial infections.

Indexed as

Adrenergic NeuronsAnimalsCell MovementChemokine CCL2CytokinesInflammationKlebsiella InfectionsKlebsiella pneumoniaeMacrophagesMast CellsMiceMice, Inbred C57BLMonocytesPeritonitisSpleenCcl2 protein, mouseChemokine CCL2Cytokines

Identifiers

PMID23543756
PMCPMC3973442
OpenAlexW2105062572

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.