Evidence map›Paper›PMID 41023910›Full record

ArticleBMC infectious diseases2025

The regulating markers for Brucella spondylitis and tuberculous spondylitis.

Wei Hu, Nianrong Han, Yanlu Liu, Fengbo Zhang, Aikeremu Wusiman, Yifei Huang

Abstract read
In one paragraph

Article in BMC infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. 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

6 authors.

Wei Hu *The Second Department of Spine, the Fourth Clinical Medical College of Xinjiang Medical University, No. 116 Huanghe Road, Urumqi, Xinjiang, 830000, China.
Nianrong Han *The Second Department of Spine, the Fourth Clinical Medical College of Xinjiang Medical University, No. 116 Huanghe Road, Urumqi, Xinjiang, 830000, China.
Yanlu LiuThe Second Department of Spine, the Fourth Clinical Medical College of Xinjiang Medical University, No. 116 Huanghe Road, Urumqi, Xinjiang, 830000, China.
Fengbo ZhangDepartment of Laboratory Medicine, the First Affiliated Hospital of Xinjiang Medical University, No. 137 Liyushan South Road, Urumqi, Xinjiang, 830000, China.
Aikeremu WusimanThe Second Department of Spine, the Fourth Clinical Medical College of Xinjiang Medical University, No. 116 Huanghe Road, Urumqi, Xinjiang, 830000, China.
Yifei HuangThe Second Department of Spine, the Fourth Clinical Medical College of Xinjiang Medical University, No. 116 Huanghe Road, Urumqi, Xinjiang, 830000, China. jerkhuang@163.com.

Funding

National Natural Science Foundation of China 81960812
6 · The paper itself

Abstract

backgroundExploring the differential mechanism between Brucella spondylitis (BS) and Tuberculous spondylitis (TS) is crucial for the full treatment and management of this disease.

methodsSpinal samples of 14 patients with BS, 13 patients with TS, and 13 controls were recruited. Among them, 4 BS patients, 3 TS patients, and 3 controls were randomly selected for high-throughput sequencing. Differential expression analysis was performed among the three groups to identify the regulatory relationships between lncRNAs and mRNAs. Weighted Gene Co-expression Network Analysis (WGCNA) and enrichment analysis were constructed for the differentially expressed mRNAs (DEmRs) and differentially expressed lncRNAs (DElncRs). Finally, experiments were conducted using the remaining samples for validation.

resultsA total of 213 DEmRs and 97 DElncRs were specific to BS, 242 DEmRs and 54 DElncRs were specific to TS. In the identified 16 co-expression modules, the black module showing the highest positive correlation with BS and the lightcyan module showing the highest positive correlation with TS. Enrichment analysis revealed that genes in the black module were primarily associated with the Toll-like receptor signaling pathway. Genes in the lightcyan module were mainly associated with Th1 and Th2 cell differentiation, as well as Th17 cell differentiation. Western blot confirmed increased TLR4 expression in BS, and flow cytometry showed elevated Th2 cells and reduced Th17 cells in TS.

conclusionCXCL8, CCL3, and CCL4L2 may be involved in the pathological process of BS through TLR4 signaling. Similarly, HLA-DRB3 and HLA-DRB1 may be involved in the pathological process of TS through the regulation of T-cell subgroups.

Indexed as

BrucellosisSpondylitisTuberculosis, SpinalAdultBiomarkersBrucellaFemaleGene Expression ProfilingGene Regulatory NetworksHumansMaleMiddle AgedRNA, Long NoncodingRNA, MessengerToll-Like Receptor 4BiomarkersRNA, Long NoncodingRNA, MessengerTLR4 protein, humanToll-Like Receptor 4Brucella spondylitisLncRNAsT cellsTLR4Tuberculous spondylitis

Identifiers

PMID41023910
PMCPMC12482795

What OpenQuestion holds

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Registered trials

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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.