Epigenetic reprogramming involved in bronchial epithelial cells memory induced by flagellin stimulation
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PROVIDER: PRJNA944248 | ENA |
REPOSITORIES: ENA
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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.
2025-08-10 | GSE227261 | GEO
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.
2025-08-10 | GSE227260 | GEO
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.
2025-08-10 | GSE227259 | GEO
Project description:Bronchial epithelial cells transcriptomics upon flagellin stimulation (Microarray)
| PRJNA944253 | ENA
Project description:Bronchial epithelial cells accessibility upon flagellin stimulation (ATAC-Seq)
| PRJNA944250 | ENA
Project description:RNAseq was used to measure the transciptional respose of human bronchial epithelium (HBE) to the bacterial component flagellin with particular emphasis on innate immunity and metabolism.
2021-01-13 | GSE164704 | GEO
Project description:Airway epithelial cells represent the first line of defense against respiratory pathogens. Flagellin drives the motility of many mucosal pathogens and has been suggested as an immune enhancing adjunctive therapeutic in infections of the airways. This study leveraged single-cell RNA sequencing to determine cell-specific effects of flagellin in primary human bronchial epithelial cells growing in air-liquid interface. Seven cell clusters were identified, including ciliated cells, ionocytes and several states of basal and secretory cells, of which only inflammatory basal cells and inflammatory secretory cells demonstrated a proportional increase in response to flagellin. Inflammatory secretory cells showed evidence of metabolic reprogramming toward aerobic glycolysis, whilst in inflammatory basal cells transcriptome profiles indicated enhanced oxidative phosphorylation. Inhibition of mTOR prevented the shift to glycolysis and reduced inflammatory gene transcription specifically in inflammatory secretory cells. This data demonstrates the functional heterogeneity of the human airway epithelium upon exposure to flagellin.
2024-09-18 | GSE272188 | GEO
Project description:Vaccine adjuvants enhance adaptive immunity to co-administered antigens. Whereas the modes of action are multiple, the activation of antigen-presenting cells (APC) like dendritic cells by adjuvants is a prerequisite. Detection of microbial signals by innate sensors like Toll-like receptors (TLR) is a major mechanism of APC activation. Most candidate or licensed vaccines assume that adjuvant activity of TLR agonists depends on direct effect on APCs. This study addressed whether TLR stimulation of non-hematopoietic cells could contribute to the adjuvant effect. Nasal administration of flagellin enhanced T cell- and antibody-mediated immunity to co-administered antigens in a TLR5-dependent but inflammasome-independent manner. We found that lung radioresistant cells were sufficient to promote immunity, thereby suggesting that direct TLR5-mediated APC stimulation is dispensable to adjuvant activity. Consistent with this, radioresistant compartment is essential to stimulate the swift TLR5-dependent transcription. The transcriptional response was restricted to the epithelial compartment and was associated to the production of a narrow set of mediators including the chemokine CCL20, known to promote APC recruitment in mucosal tissues. Besides, flagellin was rapidly degraded in lower airways and was not transported into lung parenchyma or peripheral tissues. This study therefore suggests an unexpected mechanism for how TLR agonists act as adjuvant and how epithelium is instrumental to sense and integrate microbial signals to promote adaptive immunity. In conclusion, the immune-enhancing effect of adjuvants on epithelial cells can be harnessed for improving vaccines. 1 µg of flagellin was instillated intranasally to LPS-unresponsive C3H/HeJ mice. Total lung RNA was extracted 1h later and prepare for hybridization on Affymetrix microarrays.
2013-03-22 | E-GEOD-45369 | biostudies-arrayexpress
Project description:Vaccine adjuvants enhance adaptive immunity to co-administered antigens. Whereas the modes of action are multiple, the activation of antigen-presenting cells (APC) like dendritic cells by adjuvants is a prerequisite. Detection of microbial signals by innate sensors like Toll-like receptors (TLR) is a major mechanism of APC activation. Most candidate or licensed vaccines assume that adjuvant activity of TLR agonists depends on direct effect on APCs. This study addressed whether TLR stimulation of non-hematopoietic cells could contribute to the adjuvant effect. Nasal administration of flagellin enhanced T cell- and antibody-mediated immunity to co-administered antigens in a TLR5-dependent but inflammasome-independent manner. We found that lung radioresistant cells were sufficient to promote immunity, thereby suggesting that direct TLR5-mediated APC stimulation is dispensable to adjuvant activity. Consistent with this, radioresistant compartment is essential to stimulate the swift TLR5-dependent transcription. The transcriptional response was restricted to the epithelial compartment and was associated to the production of a narrow set of mediators including the chemokine CCL20, known to promote APC recruitment in mucosal tissues. Besides, flagellin was rapidly degraded in lower airways and was not transported into lung parenchyma or peripheral tissues. This study therefore suggests an unexpected mechanism for how TLR agonists act as adjuvant and how epithelium is instrumental to sense and integrate microbial signals to promote adaptive immunity. In conclusion, the immune-enhancing effect of adjuvants on epithelial cells can be harnessed for improving vaccines.
2013-03-22 | GSE45369 | GEO