ArticlePloS one2017
Disruption of outer blood-retinal barrier by Toxoplasma gondii-infected monocytes is mediated by paracrinely activated FAK signaling.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- The Future of Protozoan Infection Research: 3D Cell Culture and beyond.ACS infectious diseases · 2026Review
- The eye as a gateway to the brain: mechanisms of ocular neuroinvasion by parasitic pathogens.GMS hygiene and infection control · 2026Article
- Retinal pigment epithelium drives macrophage migration during Toxoplasma gondii infection in vitroMemorias do Instituto Oswaldo Cruz · 2026Article
- Disruption of Epidermal Growth Factor Receptor Signaling in RPE Cells Increases Resistance to Ocular Toxoplasmosis.Investigative ophthalmology & visual science · 2025Article
- New advances in immune mechanism and treatment during ocular toxoplasmosis.Frontiers in immunology · 2024Review
- Inflammatory mechanisms contributing to retinal alterations in HIV infection and long-term ART.Southern African journal of HIV medicine · 2024Review
- From Bedside to Diagnosis: The Role of Ocular Fundus in Systemic Infections.Journal of clinical medicine · 2023Review
- Visualization of parasite dynamics in the host tissues: application of tissue transparency technology to parasite research.The Journal of veterinary medical science · 2023Review
- Type I and III interferons shape the retinal cytokine network and barrier function in anFrontiers in immunology · 2023Article
- FAF1 downregulation by Toxoplasma gondii enables host IRF3 mobilization and promotes parasite growth.Journal of cellular and molecular medicine · 2021Article
- Harmonization of Protocols for Multi-Species Organoid Platforms to Study the Intestinal Biology ofFrontiers in cellular and infection microbiology · 2020Article
- Implications of TORCH Diseases in Retinal Development-Special Focus on Congenital Toxoplasmosis.Frontiers in cellular and infection microbiology · 2020Review
- Transcriptional Analyses Identify Genes That Modulate Bovine Macrophage Response toFrontiers in cellular and infection microbiology · 2020Article
- Molecular Basis of The Retinal Pigment Epithelial Changes That Characterize The Ocular Lesion in Toxoplasmosis.Microorganisms · 2019Article
- Immunological Molecular Responses of Human Retinal Pigment Epithelial Cells to Infection WithFrontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ocular toxoplasmosis is mediated by monocytes infected with Toxoplasma gondii that are disseminated to target organs. Although infected monocytes can easily access to outer blood-retinal barrier due to leaky choroidal vasculatures, not much is known about the effect of T. gondii-infected monocytes on outer blood-retinal barrier. We prepared human monocytes, THP-1, infected with T. gondii and human retinal pigment epithelial cells, ARPE-19, grown on transwells as an in vitro model of outer blood-retinal barrier. Exposure to infected monocytes resulted in disruption of tight junction protein, ZO-1, and decrease in transepithelial electrical resistance of retinal pigment epithelium. Supernatants alone separated from infected monocytes also decreased transepithelial electrical resistance and disrupted tight junction protein. Further investigation revealed that the supernatants could activate focal adhesion kinase (FAK) signaling in retinal pigment epithelium and the disruption was attenuated by FAK inhibitor. The disrupted barrier was partly restored by blocking CXCL8, a FAK activating factor secreted by infected monocytes. In this study, we demonstrated that monocytes infected with T. gondii can disrupt outer blood-retinal barrier, which is mediated by paracrinely activated FAK signaling. FAK signaling can be a target of therapeutic approach to prevent negative influence of infected monocytes on outer blood-retinal barrier.
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