Evidence map›Paper›PMID 19497959›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009

Neutrophil chemokines and their role in IL-18-mediated increase in neutrophil O2- production and intestinal edema following alcohol intoxication and burn injury.

Suhail Akhtar, Xiaoling Li, Irshad H Chaudry, Mashkoor A Choudhry

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

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  18. Noninvasive measurement of intestinal inflammation after burn injury.Journal of burn care & research : official publication of the American Burn Association
    Article
  19. Article
  20. Inflammatory response in multiple organs in a mouse model of acute alcohol intoxication and burn injury.Journal of burn care & research : official publication of the American Burn Association
    Article
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 at 1 institution in 1 country.

Suhail AkhtarBurn and Shock Trauma Institute and Alcohol Research Program, Department of Surgery, Loyola University Medical Center, Maywood, Illinois 60153, USA.
Xiaoling Li
Irshad H Chaudry
Mashkoor A Choudhry
Loyola University Medical Center · US

Funding

Alcohol Intoxication and Postburn Intestinal ImmunityR01AA015731 · NIAAA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHOUDHRY, MASHKOOR A · 2007 to 2017
$3.8M
Interleukin-18 and Intestinal Barrier Function Following Alcohol and Burn InjuryR21AA015979 · NIAAA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI CHOUDHRY, MASHKOOR A · 2006 to 2007
$378k
NIAAA NIH HHS R01AA015731NIAAA NIH HHS R21AA015979
6 · The paper itself

Abstract

We examined the role of interleukin (IL)-18 and cytokine-induced neutrophil chemokines (CINC)-1 and CINC-3 in the neutrophil release of superoxide anion (O2-) and elastase following alcohol/ethanol (EtOH) and burn injury. Male rats (approximately 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dl before approximately 12.5% total body surface area burn or sham injury. Immediately after injury, rats were administered with anti-rat IL-18 antibody (80 microg/kg) or isotype control. After 20 min, anti-IL-18 antibody-treated rats were given either recombinant (r) rat CINC-1 or CINC-3. On day 1 after injury, the combined insult of EtOH and burn injury caused a significant increase in neutrophil elastase and O2- production as well as an increase in neutrophil accumulation, myeloperoxidase activity, and edema in the intestine. Treatment of rats with anti-IL-18 antibody normalized the above parameters. However, administration of rCINC-1 in anti-IL-18 antibody-treated rats increased the above parameters to levels similar to those observed following EtOH and burn injury. In contrast, administration of rCINC-3 did not influence the above parameters except neutrophil elastase. These findings indicate that IL-18 and CINC-1 may independently modulate neutrophil tissue-damaging actions following EtOH and burn injury. However, the finding that the treatment of rats with anti-IL-18 antibodies inhibits CINC-1 and CINC-3 supports the notion that IL-18 plays a critical role in increased neutrophil tissue-damaging action following a combined insult of EtOH intoxication and burn injury.

Indexed as

Alcoholic IntoxicationAnimalsAntibodiesBurnsChemokine CXCL1Chemokines, CXCDisease Models, AnimalEdemaInterleukin-18Intestinal DiseasesLeukocyte ElastaseMaleNeutrophilsRatsRats, Sprague-DawleyRecombinant ProteinsAntibodiesChemokine CXCL1Chemokines, CXCCxcl1 protein, ratInterleukin-18Leukocyte ElastaseRecombinant ProteinsSuperoxides

Identifiers

PMID19497959
PMCPMC2724079
OpenAlexW2166790008

What OpenQuestion holds

Textmetadata
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.