Evidence map›Paper›PMID 42749963›Full record

ReviewJournal of ophthalmic inflammation and infection2026

Putative mechanisms of ocular inflammation in syphilis.

Liam M Ashander, João M Furtado, Keryn A Williams, Giles Best, Melissa H Brown, Justine R Smith

Abstract readReview
In one paragraph

Review in Journal of ophthalmic inflammation and infection, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Liam M AshanderFlinders Health and Medical Research Institute, College of Medicine and Public Health, Flinders University, Adelaide, Australia. liam.ashander@flinders.edu.au.ORCID https://orcid.org/0000-0002-3808-9763
João M FurtadoRibeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil.
Keryn A WilliamsFlinders Health and Medical Research Institute, College of Medicine and Public Health, Flinders University, Adelaide, Australia.
Giles BestFlinders Health and Medical Research Institute, College of Medicine and Public Health, Flinders University, Adelaide, Australia.
Melissa H BrownCollege of Science and Engineering, Flinders University, Adelaide, Australia.
Justine R SmithFlinders Health and Medical Research Institute, College of Medicine and Public Health, Flinders University, Adelaide, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOcular syphilis is re-emerging globally as a cause of uveitis, with the potential for substantial vision loss. Multimodal ophthalmic imaging and advanced laboratory research can yield important information about the basic mechanisms of this infectious eye disease. REVIEW: Inflammation of the retina is a frequent manifestation of ocular syphilis. Observations from multimodal ophthalmic imaging suggest the retinal pigment epithelium and retinal vasculature are often involved. Molecular profiling of biopsies from patients with syphilis involving the eye and brain indicates multiple leucocyte subsets infiltrate the posterior eye, and highlights the role of monocytes and macrophages in promoting inflammation. Aqueous and cerebrospinal fluid samples from patients with ocular syphilis contain high levels of inflammatory mediators, including C-C motif chemokine ligand (CCL) 2, C-X-C motif chemokine ligand (CXCL) 8, interleukin (IL)-6, IL-12, and tumour necrosis factor (TNF). Macrophages and dendritic cells exposed to the causative bacterium, Treponema pallidum, increase the production of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF. Toll-like receptor activation and nuclear factor of kappa light chain enhancer of B-cells (NFκB) signalling in non-ocular human cells play prominent roles in upregulating inflammatory molecules, and altering interactions between leucocytes and epithelial or endothelial cells; similar cellular and molecular changes at the outer and inner blood-retinal barriers could contribute to retinal inflammation in ocular syphilis. Experimental evidence also indicates that T. pallidum alters intercellular junctions and transmigrates endothelial cell monolayers, potentially mediating retinal invasion.

conclusionsEvidence from multimodal ophthalmic imaging, molecular profiling in patients, and non-ocular cell infection models provides essential insights into the pathogenesis of ocular syphilis. This knowledge will target future research towards elucidating the drivers of retinal inflammation in ocular syphilis.

Indexed as

InfectionMechanismsOcular syphilisRetinaSyphilisSyphilitic uveitisTreponema pallidum

Identifiers

PMID42749963
PMCPMC13582787

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.