Evidence map›Paper›PMID 28265564›Full record

ArticleInternational journal of genomics2017

The Numerical Predominance and Large Transcriptome Differences of Neutrophils in Peripheral Blood Together Inevitably Account for a Reported Pulmonary Tuberculosis Signature.

Kang Wu, Ka-Wing Wong, Wang-Long Deng, Hao Zhang, Jing Li, Douglas B Lowrie, Xiao-Yong Fan

Abstract read
In one paragraph

Article in International journal of genomics, 2017. 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
–field-weighted citation impact
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.

  1. The Biological and Clinical Aspects of a Latent Tuberculosis Infection.Tropical medicine and infectious disease · 2022
    Review
  2. Article
  3. Review
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

7 authors.

Kang WuShanghai Public Health Clinical Center, Key Laboratory of Medical Molecular Virology of MOE/MOH, Fudan University, 2901 Caolang Road, Shanghai 201508, China; Shanghai Medical College, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China.ORCID 0000-0002-9840-7671
Ka-Wing WongShanghai Public Health Clinical Center, Key Laboratory of Medical Molecular Virology of MOE/MOH, Fudan University, 2901 Caolang Road, Shanghai 201508, China; Shanghai Medical College, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China.ORCID 0000-0001-8356-5880
Wang-Long DengState Key Laboratory of Medical Genomics, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Hao ZhangDepartment of Pathology, Qiqihar Medical University, Qiqihar 161006, China.
Jing LiDepartment of Genetics and Biochemistry, Clemson University, Clemson, SC 29634, USA.ORCID 0000-0001-5454-5135
Douglas B LowrieShanghai Public Health Clinical Center, Key Laboratory of Medical Molecular Virology of MOE/MOH, Fudan University, 2901 Caolang Road, Shanghai 201508, China; Shanghai Medical College, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China.ORCID 0000-0003-2689-9627
Xiao-Yong FanShanghai Public Health Clinical Center, Key Laboratory of Medical Molecular Virology of MOE/MOH, Fudan University, 2901 Caolang Road, Shanghai 201508, China; Shanghai Medical College, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China.ORCID 0000-0001-6654-3559

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous transcriptomic analysis revealed a 393-transcript signature (PTBsig), which is dominated by interferon inducible genes, in whole blood of pulmonary tuberculosis (PTB) patients. Comparisons with a limited set of interferon-driven genes among separated monocytes, CD4+ T cells, CD8+ T cells, and neutrophils indicated that the signature is due to changes in neutrophils, the overwhelmingly predominant cell type. By extending the analysis to the entire 393 transcripts of PTBsig and by switching the cell proportions between separated monocytes, CD4+ T cells, CD8+ T cells, and neutrophils, we create putative PTBsig for whole blood (pPTBsig) in which CD4+ or CD8+ T cells or monocytes predominated or in which the cell proportions were unchanged. These putative signatures are then compared to the actual reported PTBsig. We show that, because of their predominance in peripheral blood and their larger transcriptional responses, neutrophils were indeed almost exclusively responsible for PTBsig. We caution that the functional significance of changes in other cell types might escape notice in transcriptome analysis that is based upon whole blood.

Identifiers

PMID28265564
PMCPMC5317119

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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.