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Identification and exploration of pharmacological pyroptosis-related biomarkers of ulcerative colitis. | LitMetric

AI Article Synopsis

  • * The study identified 10 key genes related to a specific type of cell death called pyroptosis using gene expression data, suggesting these genes are linked to both UC progression and how patients respond to treatments.
  • * Results showed that macrophages are closely associated with pyroptosis in UC, and further investigation is warranted into how the interaction between macrophage and intestinal cell pyroptosis contributes to the disease and treatment effectiveness.

Article Abstract

Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD). Its etiology is unclear. Much evidence suggests that the death of abnormal intestinal epithelial cells (IECs) leads to intestinal barrier disruption, and the subsequent inflammatory response plays a vital role in UC. Pyroptosis is a form of programmed inflammatory cell death, and the role of pyroptosis in UC etiology remains to be explored. This study identified 10 hub genes in pyroptosis by gene expression profiles obtained from the GSE87466 dataset. Meanwhile, the biomarkers were screened based on gene significance (GS) and module membership (MM) through the Weighted Gene Co-Expression Network Analysis (WGCNA). The following analysis indicated that hub genes were closely associated with the UC progression and therapeutic drug response. The single-cell RNA (scRNA) sequencing data from UC patients within the GSE162335 dataset indicated that macrophages were most related to pyroptosis. Finally, the expression of hub genes and response to the therapeutic drug [5-aminosalicylic acid (5-ASA)] were verified in dextran sulfate sodium (DSS)-induced colitis mice. Our study identified as the critical pyroptosis-related biomarker in UC. The crosstalk between macrophage pyroptosis and IEC pyroptosis may play an essential role in UC, deserving further exploration.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9606687PMC
http://dx.doi.org/10.3389/fimmu.2022.998470DOI Listing

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