ArticleInvestigative ophthalmology & visual science2025
Hyperglycemia-Suppressed Acod1 Expression Contributes to Innate Immune Deficiency in Pseudomonas aeruginosa Keratitis.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Itaconate and its derivatives in human health and diseases.Signal transduction and targeted therapy · 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
5 authors.
Funding
Abstract
Purpose: Diabetes mellitus (DM) patients are at higher risk for infections, which are often more severe. This study investigated the role of aconitate decarboxylase 1 (Acod1) and its product, itaconate, in innate defense against bacterial keratitis and its impairment in type 1 DM mice. Methods: Wild-type or normal (NL), streptozotocin-induced DM, and Acod1-/- mice were inoculated with Pseudomonas aeruginosa (Pa) with or without 4-octyl itaconate (4-OI), a cell-permeable derivative of itaconate. Keratitis severity was determined by photography, clinical scores, Pa burden (cfu), and myeloperoxidase (MPO) activity. Gene expression was determined by quantitative PCR. Immune and Acod1-positive cells were determined by immunohistochemistry. Results: DM mice expressed lower levels of Acod1 in B6 mouse corneas, and Pa infection triggered its upregulation, mostly in infiltrated cells. Acod1 deficiency increased the severity of Pa keratitis and significantly augmented the expression of Il-1β, Il-1ra, and Ccl3, but not Ccl2, at 1 day post-infection (dpi). Acod1-/- increased neutrophil but decreased macrophage infiltration. 4-OI prevented Pa infection in NL corneas (P = 6.7E-05) and alleviated Pa keratitis in DM corneas (P = 0.000204) at 3 dpi. Hyperglycemia augmented Pa infection-induced Il-1β, Il-1ra, and particularly Ccl3, but not Ccl2. In DM corneas, 4-OI greatly dampened the expression of CCL3 but not CCL2, compared to DM corneas without the treatment. The presence of 4-OI significantly reduced the severity of Pa keratitis in Acod1-deficient mice. Conclusions: Acod1/itaconate is crucial for mediating protective immune responses against Pa infection in both NL and DM corneas. Acod1 activation and/or itaconate-based therapies may offer promising adjunctive treatments for microbial keratitis in patients with diabetes.
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.