Multi-model transcriptomic atlas reveals shared inflammatory programs and epithelial-immune crosstalk in chronic colitis
By
Eduardo J. Villablanca1,2,3,8,10 Send email to [email protected]
The bagel they save for the regulars. Don't skim, savour.
Summary
This study by Fransson, Sorini, et al. presents a multi-model, longitudinal transcriptomic atlas of experimental chronic colitis, integrating bulk, single-cell, and spatial transcriptomics across T cell transfer and Il10−/− spontaneous colitis models, including anti-IL-12p40 intervention. The research reveals shared inflammatory programs across models, identifies epithelial antigen presentation as a key feature, and characterizes dynamic neutrophil states. The findings link mouse models to human IBD and highlight epithelial-immune crosstalk as a potential therapeutic target for inflammatory bowel disease.
Key quotes
· 3 pulledInflammatory bowel disease (IBD) is a complex disorder that is often resistant to immunomodulatory treatments.
These well-established models exhibited conserved features of chronic inflammation, including neutrophil infiltration, and impaired tissue regeneration.
They reveal shared inflammatory programs, epithelial antigen presentation, and dynamic neutrophil states, linking mouse models to human IBD and highlighting epithelial-immune crosstalk as a therapeutic target.
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