Evidence map›Paper›PMID 20396927›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2010

Lung inflammation is induced by renal ischemia and reperfusion injury as part of the systemic inflammatory syndrome.

G Campanholle, R G Landgraf, G M Gonçalves, V N Paiva, J O Martins, P H M Wang, R M M Monteiro, R C Silva, M A Cenedeze, V P A Teixeira and 4 more

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Identifying pathophysiological bases of disease in COVID-19.Translational medicine communications · 2020
    Review
  5. Review
  6. Article
  7. Nephrogenic acute respiratory distress syndrome: A narrative review on pathophysiology and treatment.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2018
    Review
  8. Article
  9. Article
  10. Article
  11. 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

14 authors at 3 institutions in 1 country.

G CampanholleLaboratory of Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences IV, University of São Paulo, Av. Prof. Lineu Prestes, 1730, São Paulo, SP 05508-900, Brazil.
R G Landgraf
G M Gonçalves
V N Paiva
J O Martins
P H M Wang
R M M Monteiro
R C Silva
M A Cenedeze
V P A Teixeira
M A Reis
A Pacheco-Silva
S Jancar
Niels Olsen Saraiva Camara
Universidade Federal de São Paulo · BRUniversidade de São Paulo · BRUniversidade Federal do Triângulo Mineiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIschemia and reperfusion injury (IRI) are mainly caused by leukocyte activation, endothelial dysfunction and production of reactive oxygen species. Moreover, IRI can lead to a systemic response affecting distant organs, such as the lungs.

aimThe objective was to study the pulmonary inflammatory systemic response after renal IRI.

methodsMale C57Bl/6 mice were subjected to 45 min of bilateral renal ischemia, followed by 4, 6, 12, 24 and 48 h of reperfusion. Blood was collected to measure serum creatinine and cytokine concentrations. Bronchoalveolar lavage fluid (BALF) was collected to determine the number of cells and PGE(2) concentration. Expressions of iNOS and COX-2 in lung were determined by Western blot. Gene analyses were quantified by real time PCR.

resultsSerum creatinine increased in the IRI group compared to sham mainly at 24 h after IRI (2.57 +/- 0.16 vs. 0.43 +/- 0.07, p < 0.01). The total number of cells in BAL fluid was higher in the IRI group in comparison with sham, 12 h (100 x 10(4) +/- 15.63 vs. 18.1 x 10(4) +/- 10.5, p < 0.05) 24 h (124 x 10(4) +/- 8.94 vs. 23.2 x 10(4) +/- 3.5, p < 0.05) and 48 h (79 x 10(4) +/- 15.72 vs. 22.2 x 10(4) +/- 4.2, p < 0.05), mainly by mononuclear cells and neutrophils. Pulmonary COX-2 and iNOS were up-regulated in the IRI group. TNF-alpha, IL-1beta, MCP-1, KC and IL-6 mRNA expression were up-regulated in kidney and lungs 24 h after renal IRI. ICAM-1 mRNA was up-regulated in lungs 24 h after renal IRI. Serum TNF-alpha, IL-1beta and MCP-1 and BALF PGE(2) concentrations were increased 24 h after renal IRI.

conclusionRenal IRI induces an increase of cellular infiltration, up-regulation of COX-2, iNOS and ICAM-1, enhanced chemokine expression and a Th1 cytokine profile in lung demonstrating that the inflammatory response is indeed systemic, possibly leading to an amplification of renal injury.

Indexed as

PneumoniaReperfusion InjurySystemic Inflammatory Response SyndromeAnimalsBronchoalveolar Lavage FluidChemokinesCyclooxygenase 2CytokinesIntercellular Adhesion Molecule-1KidneyMaleMiceMice, Inbred C57BLNitric Oxide Synthase Type IIChemokinesCyclooxygenase 2CytokinesIntercellular Adhesion Molecule-1Nitric Oxide Synthase Type IIPTGS2 protein, human

Identifiers

PMID20396927
OpenAlexW1993375614

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.