ABSTRACT: Genome-wide transcriptional analysis of flagellin induced reprogramming in mouse corneal epithelial cells in response to Pseudomonas aeruginosa
Project description:We previously showed that pre-exposure of the cornea to TLR5 ligand flagellin induces profound mucosal innate protection against pathogenic microbes by reprogramming gene expression. To date, there was no genome-wide cDNA array to detect full scale of flagellin mediated reprogramming of gene expression in mucosal surface epithelial cells. Taking advantage of readily accessible, easily procurable epithelial cell population, this study is the first report to use genome-wide cDNA microarray approach to document genes associated with flagellin-induced protection against Pseudomonas aeruginosa infection in corneal epithelial cells (CECs). Total RNA obtained from isolated mouse corneal epithelial cells of the control (cells scrapped off from the corneas without infection), Pseudomonas aeruginosa infected (6 h post infection) and flagellin pretreated (24 h), followed by Pseudomonas aeruginosa infection (6 h).
Project description:We previously showed that pre-exposure of the cornea to TLR5 ligand flagellin induces profound mucosal innate protection against pathogenic microbes by reprogramming gene expression. To date, there was no genome-wide cDNA array to detect full scale of flagellin mediated reprogramming of gene expression in mucosal surface epithelial cells. Taking advantage of readily accessible, easily procurable epithelial cell population, this study is the first report to use genome-wide cDNA microarray approach to document genes associated with flagellin-induced protection against Pseudomonas aeruginosa infection in corneal epithelial cells (CECs).
Project description:Innate immune memory is a new concept describing ability of innate myeloid and lymphoid cells to gain memory characteristics after transient stimulation, resulting in an nonspecific modified response upon secondary challenge. In recent work, we demonstrated that bronchial epithelial cells that are non immune cells, the first immune cells of the lower respiratory tract to encounter pathogens were capable of innate immune memory after pre-exposure to Pseudomonas aeruginosa flagellin. In the present study we identified chromatin modifications induced by flagellin pre-exposure that sustain reprogramming of transcriptional patterns. We researched chromatin structure modifications responsible for the modulation of gene expression and thus of innate memory induced by the exposure of cells to flagellin.
Project description:Innate immune memory is a new concept describing ability of innate myeloid and lymphoid cells to gain memory characteristics after transient stimulation, resulting in an nonspecific modified response upon secondary challenge. In recent work, we demonstrated that bronchial epithelial cells, non immune cells, that are the first immune cells of the lower respiratory tract to encounter pathogens were capable of innate immune memory after pre-exposure to Pseudomonas aeruginosa flagellin. In the present study we identified chromatin modifications induced by flagellin pre-exposure that sustain reprogramming of transcriptional patterns. We researched chromatin structure modifications responsible for the modulation of gene expression and thus of innate memory induced by the exposure of cells to flagellin.
Project description:Innate immune memory is a new concept describing ability of innate myeloid and lymphoid cells to gain memory characteristics after transient stimulation, resulting in an nonspecific modified response upon secondary challenge. In recent work, we demonstrated that bronchial epithelial cells, non immune cells, that are the first immune cells of the lower respiratory tract to encounter pathogens were capable of innate immune memory after pre-exposure to Pseudomonas aeruginosa flagellin. In the present study we identified chromatin modifications induced by flagellin pre-exposure that sustain reprogramming of transcriptional patterns. We researched chromatin structure modifications responsible for the modulation of gene expression and thus of innate memory induced by the exposure of cells to flagellin.
Project description:Direct interactions between microorganisms and host epithelial cells play a critical role in ocular surface homeostasis and disease. In this study, human corneal epithelial cells (HCE-2) were directly exposed to either Pseudomonas aeruginosa or Staphylococcus epidermidis. RNA sequencing was performed to characterize transcriptional changes induced by direct bacterial contact compared with untreated control cells. Article available: https://doi.org/10.3389/fcimb.2026.1899147
Project description:Extracellular vesicles released by bacteria are important mediators of host-microbe communication. In this study, human corneal epithelial cells (HCE) were exposed to extracellular vesicles derived from Pseudomonas aeruginosa or Staphylococcus epidermidis. RNA sequencing was performed to characterize transcriptional changes induced by bacterial vesicles compared with untreated control cells. This dataset contains transcriptomic profiles from control cells and cells exposed to bacterial extracellular vesicles. Article available: https://doi.org/10.3389/fcimb.2026.1899147
Project description:Recombinant protein of Pseudomonas aeruginosa hook protein FlgE was added to cultured human corneal epithelial cell line for 4 hours and the mRNA expression profiling was performed using Agilent 8*60K array and dual labeling.
Project description:Recombinant protein of Pseudomonas aeruginosa hook protein FlgE was added to cultured human corneal epithelial cell line for 4 hours and the mRNA expression profiling was performed using Agilent 8*60K array and dual labeling. Three triplicates were included for FlgE treatment and PBS control respectively, thus producing three pairs of samples for array, namely E1PBS1, E2PBS2, E3PBS3.
Project description:Purpose: To determine effects of arsenic on gene expression in polarized primary human bronchial epithelial (HBE) cells and impact on transcriptional response to Pseudomonas aeruginosa infection Methods: mRNA profiles of HBE cells from 6 donors exposed to 0, 5, 10 or 50 ug/L total arsenic +/- Pseudomonas aeruginosa (48 samples) were generated using Illumina sequencing, aligned in CLC Genomics workbench and analyzed for DE in EdgeR Findings: 20-30 million reads were mapped per sample and transcripts were identifed that were significantly differentially expressed in response to arsenic and Pseudomonas aeruginosa
