Evidence map›Paper›PMID 39574316›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

A Study on the Inflammatory Response of the Brain in Neurosyphilis.

Qiyu Zhang, Jie Ma, Jia Zhou, Hanlin Zhang, Mansheng Li, Huizi Gong, Yujie Wang, Heyi Zheng, Jun Li, Ling Leng

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Putative mechanisms of ocular inflammation in syphilis.Journal of ophthalmic inflammation and infection · 2026
    Review
  2. Infection and immunity · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. A Study on the Inflammatory Response of the Brain in Neurosyphilis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Article
  8. 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

10 authors.

Qiyu ZhangStem cell and Regenerative Medicine Lab, Institute of Clinical Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.
Jie MaState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Jia ZhouStem cell and Regenerative Medicine Lab, Institute of Clinical Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.
Hanlin ZhangDepartment of Dermatology, Institute of Clinical Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, 100730, China.
Mansheng LiState Key Laboratory of Medical Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, 102206, China.
Huizi GongDepartment of Dermatology, Institute of Clinical Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, 100730, China.
Yujie WangStem cell and Regenerative Medicine Lab, Institute of Clinical Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.
Heyi ZhengDepartment of Dermatology, Institute of Clinical Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, 100730, China.
Jun LiDepartment of Dermatology, Institute of Clinical Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, 100730, China.
Ling LengStem cell and Regenerative Medicine Lab, Institute of Clinical Medicine, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100730, China.ORCID https://orcid.org/0000-0002-6519-012X

Funding

Beijing Municipal Science & Technology Commission Z231100007223009CAMS Innovation Fund for Medical Sciences (CIFMS) 2023-I2M-3-002CAMS Innovation Fund for Medical Sciences (CIFMS) 2023-I2M-QJ-001National High Level Hospital Clinical Research Funding 2022-PUMCH-A-022National Natural Science Foundation of China 82341079
6 · The paper itself

Abstract

Neurosyphilis (NS) is a clinical condition caused by infection of the central nervous system (CNS) by Treponema pallidum (Tp) that can lead to asymptomatic meningitis and more serious neurological diseases, such as dementia and blindness. However, current studies on the pathogenesis of NS are limited. Here, through the integration analysis of proteomics and single-cell transcriptomics, Toll-like/NF-κB signaling is identified as the key pathway involved in CNS damage caused by Tp. Moreover, monocyte-derived macrophages are key cells involved in the inflammatory response to Tp in the CNS of NS patients. In addition, it is found that inflammatory cells in peripheral blood may cause neurological damage through disruption of the blood‒brain barrier (BBB) in individuals with NS. Notably, activation of the Toll-like/NF-κB signaling pathway, as well as dysregulation of neural function, is likewise validated in an in vitro NS brain organoid model. In conclusion, the results revealed the mechanisms of inflammation-mediated brain injury in Tp-induced NS and provided new ideas for the clinical treatment of Tp infection.

Indexed as

BrainInflammationNeurosyphilisBlood-Brain BarrierFemaleHumansMacrophagesMaleNF-kappa BProteomicsSignal TransductionTreponema pallidumNF-kappa Bblood‒brain barrierinflammation‐mediated brain injuryneurosyphilisproteomicssingle‐cell transcriptomics

Identifiers

PMID39574316
PMCPMC11792053

What OpenQuestion holds

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LicenceCC BY
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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.