Evidence map›Paper›PMID 18453614›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Heme oxygenase-1 protects against neutrophil-mediated intestinal damage by down-regulation of neutrophil p47phox and p67phox activity and O2- production in a two-hit model of alcohol intoxication and burn injury.

Xiaoling Li, Martin G Schwacha, Irshad H Chaudry, Mashkoor A Choudhry

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 65 citations in OpenAlex.

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  11. Recipient HO-1 inducibility is essential for posttransplant hepatic HO-1 expression and graft protection: From bench-to-bedside.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019
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  16. Higenamine regulates Nrf2-HO-1-Hmgb1 axis and attenuates intestinal ischemia-reperfusion injury in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015
    Article
  17. Review
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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

4 authors at 1 institution in 1 country.

Xiaoling LiCenter for Surgical Research, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Martin G Schwacha
Irshad H Chaudry
Mashkoor A Choudhry
University of Alabama at Birmingham · 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 R01 AA015731NIAAA NIH HHS R01 AA 015731-01A2NIAAA NIH HHS R21 AA015979NIAAA NIH HHS R21 AA 015979-01A1
6 · The paper itself

Abstract

Heme oxygenase-1 (HO-1) has been demonstrated to protect against tissue injury. Furthermore, HO-1 is also shown to be antioxidant. Our recent findings indicate that acute alcohol (EtOH) intoxication exacerbates postburn intestinal and lung tissue damage, and this was found to be neutrophil dependent. Because neutrophil-mediated tissue injury involves the release of superoxide anions (O(2)(-)), the present study examined the role of HO-1 in neutrophil O(2)(-) production following EtOH and burn injury. Furthermore, we investigated whether HO-1 antioxidant properties are mediated via modulation of p47(phox) and/or p67(phox) proteins. Male rats (approximately 250 g) were gavaged with EtOH to achieve a blood EtOH level of approximately 100 mg/dL before burn or sham injury (approximately 12.5% total body surface area). Some rats were treated with HO-1 activator cobalt protoporphyrin IX chloride (Copp; 25 mg/kg body weight) at the time of injury. On day 1 after injury, we found that EtOH combined with burn injury significantly increased neutrophil O(2)(-) production and p47(phox) and p67(phox) activation and decreased caspase-3 activity and apoptosis. This was accompanied with a decrease in neutrophil HO-1 levels. The treatment of animals with HO-1 activator Copp normalized neutrophil HO-1, O(2)(-), p47(phox), and p67(phox) following EtOH and burn injury. The expression of caspase-3, however, was further decreased in Copp-treated sham and EtOH plus burn groups. Moreover, Copp treatment also prevented the increase in intestinal edema and permeability following EtOH and burn injury. Altogether, these findings provide a new insight into the mechanism by which HO-1 regulates neutrophil O(2)(-) production and protect the intestine from damage following EtOH and burn injury.

Indexed as

Alcoholic IntoxicationAnimalsApoptosisBlotting, WesternBurnsCaspase 3Down-RegulationEnzyme ActivationHeme Oxygenase-1IntestinesMaleNADPH OxidasesNeutrophilsPhosphoproteinsProtoporphyrinsRatsCaspase 3cobaltiprotoporphyrinHeme Oxygenase-1NADPH Oxidasesneutrophil cytosol factor 67Kneutrophil cytosolic factor 1PhosphoproteinsProtoporphyrinsSuperoxides

Identifiers

PMID18453614
PMCPMC3065786
OpenAlexW2114533098

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.