Evidence map›Paper›PMID 22089201›Full record

ArticleShock (Augusta, Ga.)2012

Proinflammatory chemokines in the intestinal lumen contribute to intestinal dysfunction during endotoxemia.

Dennis I Sonnier, Stephanie R Bailey, Rebecca M Schuster, Matthew M Gangidine, Alex B Lentsch, Timothy A Pritts

Abstract read
In one paragraph

Article in Shock (Augusta, Ga.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

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  14. Live and heat-killed Lactobacillus rhamnosus GG upregulate gene expression of pro-inflammatory cytokines in 5-fluorouracil-pretreated Caco-2 cells.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2014
    Article
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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

6 authors at 2 institutions in 1 country.

Dennis I SonnierDepartment of Surgery, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267, USA.
Stephanie R Bailey
Rebecca M Schuster
Matthew M Gangidine
Alex B Lentsch
Timothy A Pritts
University of Cincinnati Medical Center · USUniversity of Cincinnati · US

Funding

Effects of Damage Control Resuscitation on the Inflammatory Response to HemorrhagK08GM088589 · NIGMS · UNIVERSITY OF CINCINNATI · PI PRITTS, TIMOTHY A · 2010 to 2012
$397k
NIGMS NIH HHS K08 GM088589
6 · The paper itself

Abstract

Intestinal failure is common in patients with septic shock, with dysfunction of the gut often manifesting as both a cause and consequence of their critical illness. Most studies investigating the pathogenesis of intestinal failure focus on the systemic aspect, although few data examine the inflammatory signaling in the intestinal lumen. Having previously demonstrated apical/luminal chemokine secretion in an in vitro model of intestinal inflammation, we hypothesized that endotoxemia would induce secretion of proinflammatory chemokines into the intestinal lumen. In addition, we examined the contribution of these mediators to intestinal dysmotility. C57/BL6 male mice were injected intraperitoneally with LPS. Serum, intestinal tissue, and intestinal luminal contents were harvested for cytokine analysis. For intestinal motility studies, a transit assay was performed after oral gavage of chemokines. Caco-2 cells grown on Transwell culture inserts were used to examine the role of the intestinal epithelium in chemokine secretion. Monocyte chemoattractant protein 1 (MCP-1/CCL2) and macrophage-derived chemokine (MDC/CCL22) were secreted into the lumen of multiple segments of the gut during endotoxemia in mice. In vitro work showed that the intestinal epithelium participates in monocyte chemoattractant protein 1 and MDC secretion and expresses the CCR2 and CCR4 receptors for these chemokines. Intestinal transit studies show that oral gavage of MDC results in impaired gut motility. This study demonstrates that the intestinal lumen is an active compartment in the gut's inflammatory response. Proinflammatory chemokines are secreted into the intestinal lumen during endotoxemia. These intraluminal chemokines contribute to intestinal dysmotility, complicating intestinal failure.

Indexed as

Gene Expression RegulationAnimalsCaco-2 CellsChemokine CCL2Chemokine CCL22Disease Models, AnimalEndotoxemiaHumansIntestinal DiseasesIntestinal MucosaLipopolysaccharidesMaleMiceReceptors, CCR2Receptors, CCR4Ccl22 protein, mouseCcl2 protein, mouseCcr2 protein, mouseCcr4 protein, mouseChemokine CCL2Chemokine CCL22lipopolysaccharide, Escherichia coli O111 B4LipopolysaccharidesReceptors, CCR2Receptors, CCR4

Identifiers

PMID22089201
PMCPMC4623563
OpenAlexW1988686056

What OpenQuestion holds

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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.