Evidence map›Paper›PMID 26484252›Full record

ArticleGenomics data2015

Gene expression profiling of Gram-negative bacteria-induced inflammation in human whole blood: The role of complement and CD14-mediated innate immune response.

Corinna Lau, Ole Kristoffer Olstad, Marit Holden, Ståle Nygård, Hilde Fure, Knut Tore Lappegård, Ole-Lars Brekke, Terje Espevik, Eivind Hovig, Tom Eirik Mollnes

Open access · goldAbstract read
In one paragraph

Article in Genomics data, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. 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

10 authors at 4 institutions in 1 country.

Corinna LauResearch Laboratory, Nordland Hospital, Bodø, Norway.
Ole Kristoffer OlstadDepartment of Medical Biochemistry, Oslo University Hospital, Ullevaal, Oslo, Norway.
Marit HoldenNorwegian Computing Center, Oslo, Norway.
Ståle NygårdDepartment of Informatics, University of Oslo, Oslo, Norway ; Bioinformatics Core Facility and Institute for Medical Informatics, Oslo University Hospital, Oslo, Norway.
Hilde FureResearch Laboratory, Nordland Hospital, Bodø, Norway.
Knut Tore LappegårdInstitute of Clinical Medicine, University of Tromsø, Tromsø, Norway ; Division of Medicine, Nordland Hospital, Bodø, Norway.
Ole-Lars BrekkeResearch Laboratory, Nordland Hospital, Bodø, Norway ; Faculty of Health Sciences, K.G. Jebsen TREC, University of Tromsø, Tromsø, Norway.
Terje EspevikCenter of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Eivind HovigDepartment of Tumor Biology, Institute for Cancer Research, Oslo University Hospital, Oslo, Norway ; Department of Cancer Genetics and Informatics, Oslo University Hospital, Oslo, Norway.
Tom Eirik MollnesResearch Laboratory, Nordland Hospital, Bodø, Norway ; Faculty of Health Sciences, K.G. Jebsen TREC, University of Tromsø, Tromsø, Norway ; Center of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway ; Department of Immunology, Oslo University Hospital, K.G. Jebsen IRC, University of Oslo, Oslo, Norway.
Nordland Hospital · NONorwegian University of Science and Technology · NONorwegian Computing Center · NOOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-sterile pathogen-induced sepsis and sterile inflammation like in trauma or ischemia-reperfusion injury may both coincide with the life threatening systemic inflammatory response syndrome and multi-organ failure. Consequently, there is an urgent need for specific biomarkers in order to distinguish sepsis from sterile conditions. The overall aim of this study was to uncover putative sepsis biomarkers and biomarker pathways, as well as to test the efficacy of combined inhibition of innate immunity key players complement and Toll-like receptor co-receptor CD14 as a possible therapeutic regimen for sepsis. We performed whole blood gene expression analyses using microarray in order to profile Gram-negative bacteria-induced inflammatory responses in an ex vivo human whole blood model. The experiments were performed in the presence or absence of inhibitors of complement proteins (C3 and CD88 (C5a receptor 1)) and CD14, alone or in combination. In addition, we used blood from a C5-deficient donor. Anti-coagulated whole blood was challenged with heat-inactivated Escherichia coli for 2 h, total RNA was isolated and microarray analyses were performed on the Affymetrix GeneChip Gene 1.0 ST Array platform. The initial experiments were performed in duplicates using blood from two healthy donors. C5-deficiency is very rare, and only one donor could be recruited. In order to increase statistical power, a technical replicate of the C5-deficient samples was run. Subsequently, log2-transformed intensities were processed by robust multichip analysis and filtered using a threshold of four. In total, 73 microarray chips were run and analyzed. The normalized and filtered raw data have been deposited in NCBI's Gene Expression Omnibus (GEO) and are accessible with GEO Series accession number GSE55537. Linear models for microarray data were applied to estimate fold changes between data sets and the respective multiple testing adjusted p-values (FDR q-values). The interpretation of the data has been published by Lau et al. in an open access article entitled "CD14 and Complement Crosstalk and Largely Mediate the Transcriptional Response to Escherichia coli in Human Whole Blood as revealed by DNA Microarray" (Lau et al., 2015).

Indexed as

Escherichia coliHuman whole bloodInflammationInnate immunityMicroarray

Identifiers

PMID26484252
PMCPMC4583639
OpenAlexW2139960259

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.