ArticleFrontiers in cellular and infection microbiology2025
Roles played by IL-8 in altering dynamics of trabecular meshwork cells after human cytomegalovirus infection.
Article in Frontiers in cellular and infection microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Cytomegalovirus Infection of the Anterior Segment: Corneal Endotheliitis and Secondary Glaucoma.Pathogens (Basel, Switzerland) · 2026Review
- Dual immune armies in glaucoma: microglia and monocyte-derived macrophages.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Open-angle glaucoma (OAG) is the leading cause of blindness worldwide. Human cytomegalovirus (HCMV) is known to infect the trabecular meshwork cells (HTMCs) and corneal endothelial cells leading to chronic and recurrent elevations of the intraocular pressure (IOP) as secondary glaucoma. To investigate how HCMV affects the function of HTMCs, we analyzed the effects of HCMV infection on cultured HTMCs infected with the endothelial-adapted strain, TB40/E, of HCMV. We studied the induced molecular mechanisms focusing on the OAG-associated chemokines, IL-8 and CCL2. The HTMCs were analyzed for transcriptome changes using RNAseq analysis. Our results showed that HCMV infection activated interferon signaling and significantly increased the expression of IL-8 and CCL2. The IL-8-responsive transcriptional pathway was analyzed by using a CXCR2 antagonist which is associated with cellular movement and development of the hematological system. In contrast, the CCL2-sensitive pathway, assessed using a CCR2 antagonist, was linked to olfactory receptor signaling and keratinization. HCMV infection activated cell motility with the formation of lamellipodia and filopodia. The infection-induced activation of cell motility was dependent on both CXCR2 and CCR2, and IL-8 stimulated filopodia-mediated cell motility. HCMV infection also induced cell contraction that was dependent on CXCR2, but not on CCR2, and it involved the activation of Rac1/Cdc42. These results suggest that HCMV infection altered the cytoskeletal dynamics and contraction of the HTMCs in a CCR2- and CXCR2-dependent manner. These changes have the potential of causing an increase in the resistance to aqueous humor outflow in HCMV-associated anterior uveitis and corneal endotheliitis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.