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Conditional Reprogramming of Pediatric Human Esophageal Epithelial Cells for Use in Tissue Engineering and Disease Investigation
Published on: March 22, 2017
Disease-stage-specific immunometabolic remodeling in pediatric obstructive sleep apnea: a single-cell transcriptomic
Qin Yang1,2, Yunfei Cui1, Xiao Huang1
1Department of Sleep Medicine Center, Shenzhen Children's Hospital, Shenzhen, 518038, China.
Insights
Enlarged adenoids in children can cause obstructive sleep apnea (OSA), impairing immunity. This study reveals disrupted cellular communication and immune cell function in severe OSA, identifying HIF1A signaling as a potential therapeutic target.
Area of Science:
- Immunology
- Genomics
- Pediatrics
Background:
- Hypertrophied adenoids in children can lead to obstructive sleep apnea (OSA), impacting growth and immunity.
- The underlying mechanisms of adenoid pathological transformation and their immune consequences in OSA are not fully understood.
Purpose of the Study:
- To investigate the single-cell transcriptomic and immune repertoire changes in adenoids during the progression of OSA.
- To identify molecular pathways and cellular interactions involved in OSA-related adenoid dysfunction.
Main Methods:
- Single-cell RNA sequencing and immune repertoire profiling of adenoids from children with varying degrees of OSA.
- Analysis of transcriptional regulatory networks, signaling pathways (Hippo, Notch, Wnt), and intercellular communication.
Main Results:
- Significant alterations in functional modules and transcriptional networks were observed with increasing OSA severity.
- Severe OSA was associated with downregulated energy synthesis, compromised T-cell and B-cell immunity, and reduced antigen processing.
- HIF1A-mediated hypoxic signaling was implicated in the downregulation of key immune components like HLA and interferon.
Conclusions:
- The study provides a comprehensive atlas of cellular and molecular changes in adenoids associated with OSA progression.
- Dysfunctional immune responses and impaired cell-cell communication characterize severe OSA in children.
- Targeting HIF1A-mediated hypoxic signaling presents a potential therapeutic strategy for pediatric OSA.
Abstract:
Hypertrophied adenoids in children can impair breathing and lead to obstructive sleep apnea (OSA), often accompanied by abnormal growth and weakened stamina and immunity. However, the cause of the pathological transformation in these originally immune-enhancing lymphoid tissues remains unclear. Our study provides the first single cell transcriptomic and immune repertoire atlas of adenoids from normal snoring to mild, moderate, and severe OSA, and identified markedly asynchronous functional modules, transcriptional regulatory networks and intercellular communications during the progression of OSA. Children with severe OSA exhibited exhibit active Hippo, Notch, and Wnt signaling, alongside significant downregulation of energy synthesis. Analysis revealed compromised T-cell and B-cell immunity, as well as reduced antigen processing by innate immune cells, coupled with diminished cell-cell communication in severe OSA group. T-cell receptor and B-cell receptor sequencing results also support more infection imprints and abnormal germinal centers and antibody class switching. Mechanistically, HIF1A-mediated hypoxic signaling likely drives the downregulation of key immune components (including HLA and interferon molecules), positioning it as a promising therapeutic target for OSA.
