Investigative ophthalmology & visual science · 2026
Acute Inflammation Drives Corneal Pathological Regeneration.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Han Zhuo, Guo Huizhen, Wang Bofeng, Zhu Yongxu, Zhao Xin, Chen Jialin, Mo Kunlun, Tan Jieying, Ji Jianping, Ouyang Hong, Li Mingsen
Аннотация
PURPOSE: This study aimed to characterize transcriptional and epigenetic remodeling in the cornea induced by acute inflammation.
METHODS: Limbal-corneal tissues were collected on days 5 and 10 after intrastromal administration of lipopolysaccharide or PBS. ScRNA-seq and scATAC-seq were used to delineate the transcriptomic and epigenomic atlas of the inflamed cornea, following the Seurat and Signac pipelines. Immunofluorescence was performed to assess changes in corneal epithelial markers and immune cell infiltration.
RESULTS: We identified 16 cell clusters, including ten epithelial cell subpopulations, keratocytes, fibroblasts, corneal endothelial cells, blood vessel cells, lymphatic vessel cells, and immune cells. Lipopolysaccharide induced the infiltration of five major immune cell types: neutrophils, MHC-II⁻ macrophages, MHC-II⁺ macrophages, T cells, and natural killer cells. We characterized gene expression and chromatin accessibility dynamics across all cell types during the inflammatory response, revealing cell-type-specific gene regulatory elements and cis-regulatory chromatin interactions. Regulon activity and motif accessibility analyses identified critical transcription factors that drive distinct inflammatory response programs. Inflammation was found to inhibit limbal stem/progenitor cell differentiation. CellChat analysis revealed a set of secreted intercellular crosstalk signals among all cell types.
CONCLUSIONS: Our work provides a comprehensive, time-resolved single-cell transcriptomic and epigenomic atlas of the inflamed cornea, defining cellular functional heterogeneity, cis-regulatory networks, and intercellular communication during corneal pathological regeneration. These findings offer valuable insights into corneal pathology.
METHODS: Limbal-corneal tissues were collected on days 5 and 10 after intrastromal administration of lipopolysaccharide or PBS. ScRNA-seq and scATAC-seq were used to delineate the transcriptomic and epigenomic atlas of the inflamed cornea, following the Seurat and Signac pipelines. Immunofluorescence was performed to assess changes in corneal epithelial markers and immune cell infiltration.
RESULTS: We identified 16 cell clusters, including ten epithelial cell subpopulations, keratocytes, fibroblasts, corneal endothelial cells, blood vessel cells, lymphatic vessel cells, and immune cells. Lipopolysaccharide induced the infiltration of five major immune cell types: neutrophils, MHC-II⁻ macrophages, MHC-II⁺ macrophages, T cells, and natural killer cells. We characterized gene expression and chromatin accessibility dynamics across all cell types during the inflammatory response, revealing cell-type-specific gene regulatory elements and cis-regulatory chromatin interactions. Regulon activity and motif accessibility analyses identified critical transcription factors that drive distinct inflammatory response programs. Inflammation was found to inhibit limbal stem/progenitor cell differentiation. CellChat analysis revealed a set of secreted intercellular crosstalk signals among all cell types.
CONCLUSIONS: Our work provides a comprehensive, time-resolved single-cell transcriptomic and epigenomic atlas of the inflamed cornea, defining cellular functional heterogeneity, cis-regulatory networks, and intercellular communication during corneal pathological regeneration. These findings offer valuable insights into corneal pathology.