Alterations in the Ocular Surface Microbiome in Traumatic Corneal Ulcer Patients
Corneal ulcers are a common eye inflammatory disease that can cause visual impairment or even blindness if not treated promptly. Ocular trauma is a major risk factor for corneal ulcers, and corneal trauma in agricultural work can rapidly progress to corneal ulcers. This study aims to evaluate the ch...
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Veröffentlicht in: | Investigative ophthalmology & visual science 2020-06, Vol.61 (6), p.35-35 |
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Zusammenfassung: | Corneal ulcers are a common eye inflammatory disease that can cause visual impairment or even blindness if not treated promptly. Ocular trauma is a major risk factor for corneal ulcers, and corneal trauma in agricultural work can rapidly progress to corneal ulcers. This study aims to evaluate the changes in the ocular surface (OS) microbiome of patients with traumatic corneal ulcer (TCU).
Among 20 healthy control (HC) subjects and 22 patients with TCU, 42 eyes were examined to investigate the OS microbial flora using metagenomic shotgun sequencing.
At the taxonomic composition level, our findings showed that dysbiosis (alterations in richness and community structure) occurs in the OS microbiome of patients with TCU. Notably, Pseudomonas was present at a greater than 30% relative abundance in all individuals in the TCU group. At the species level, the abundance of Pseudomonas fluorescens and Pseudomonas aeruginosa was significantly elevated in the TCU group compared to the HC group. At the functional level, we identified significant differences in the HC and TCU groups. We observed that inflammation-related pathways involved in bacterial chemotaxis, flagellar assembly, and biofilm formation were significantly more abundant in the TCU group. Besides, the pathways related to biosynthesis, degradation, and metabolism were also increased significantly in the TCU group.
These findings indicate an altered OS microbiome in the affected eyes of patients with TCU. Further research is needed to determine whether these alterations contribute to the pathogenesis of TCU or impact disease progression. |
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ISSN: | 1552-5783 0146-0404 1552-5783 |
DOI: | 10.1167/iovs.61.6.35 |