Putative mechanisms of ocular inflammation in syphilis.
Overview
- Flinders Health and Medical Research Institute, College of Medicine and Public Health, Flinders University, Adelaide, Australia
- Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, Brazil
- College of Science and Engineering, Flinders University, Adelaide, Australia
- ARC Training Centre for Biofilm Research and Innovation, Flinders University, Adelaide, Australia
Abstract
Background: Ocular 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.
Conclusions: Evidence 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.
Supplementary Information: The online version contains supplementary material available at https://
Reproduced under the paper's license (CC BY), from the paper cited above.
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Data
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- figshare:33870333, at figshare; found in DataCite
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Reproduced under the paper's license (CC BY), from the paper cited above.
Versions
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Version 3, 28 September 2026
- Funding: added Flinders University; Medical Research Council; National Health and Medical Research Council: 2025222
Version 1, 27 September 2026: the first record
Recorded: type, language, journal, volume, issue, pages, dates, 6 authors, 7 keywords, 253 references.
Cite
This paper
Ashander, L. M., Furtado, J. M., Williams, K. A., Best, G., Brown, M. H., & Smith, J. R. (2026). Putative mechanisms of ocular inflammation in syphilis. Journal of ophthalmic inflammation and infection, 16(1), 57. https://
BibTeX
@article{ashander2026put
author = {Ashander, Liam M and Furtado, João M and Williams, Keryn A and Best, Giles and Brown, Melissa H and Smith, Justine R},
title = {{Putative mechanisms of ocular inflammation in syphilis}},
journal = {Journal of ophthalmic inflammation and infection},
year = {2026},
month = sep,
volume = {16},
number = {1},
pages = {57},
publisher = {Springer},
issn = {1869-5760},
doi = {10.1186/
url = {https://
pmid = {42749963},
pmcid = {PMC13582787}
}
RIS
TY - JOUR
AU - Ashander, Liam M
AU - Furtado, João M
AU - Williams, Keryn A
AU - Best, Giles
AU - Brown, Melissa H
AU - Smith, Justine R
TI - Putative mechanisms of ocular inflammation in syphilis
T2 - Journal of ophthalmic inflammation and infection
J2 - J Ophthalmic Inflamm Infect
PY - 2026
DA - 2026/
VL - 16
IS - 1
SP - 57
SN - 1869-5760
PB - Springer
DO - 10.1186/
UR - https://
LA - en
ER -
CSL-JSON
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