ArticleFrontiers in immunology2026
Single-nucleus and spatial transcriptomics reveal intestinal cellular heterogeneity, differentiation, and cell communication mechanisms in SAP-induced intestinal injury.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- From metabolites to membrane vesicles: Unifying gut microbial signals in obesity, t2dm, and MASLD.World journal of microbiology & biotechnology · 2026Review
- Gut microbiota-host co-metabolism in hypertriglyceridemia-associated acute pancreatitis: from causality to precision intervention.Frontiers in immunology · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
Background: Acute pancreatitis (AP) ranges from mild to severe, and severe disease frequently causes multi-organ damage, with intestinal injury being a major complication. The mechanisms underlying SAP-induced intestinal injury remain unclear, particularly regarding spatial cellular reorganization and functional interactions. Methods: This study constructed a severe acute pancreatitis (SAP) rat model and employed single-nucleus RNA sequencing (snRNA-seq) and spatial transcriptome sequencing (stRNA-seq) technologies to systematically analyze the dynamic changes in intestinal cellular composition, spatial distribution, and function during SAP-induced intestinal injury. Results: snRNA-seq identified 18 major ileal cell populations spanning epithelial, immune, stem/TA, and stromal compartments. SAP was associated with compositional remodeling characterized by downward trends in Lgr5 Conclusions: Integrated single-nucleus and spatial transcriptomics reveal that SAP is accompanied by spatially organized ileal remodeling, epithelial immune-interacting rewiring, and altered neighborhood architecture, together with an ECM-centered FN1 signaling axis and attenuated Hmga2/Myb-associated regulatory programs in stem compartments. These findings provide a spatially informed cellular framework and generate testable hypotheses for mechanisms underlying impaired epithelial regeneration during SAP-associated intestinal injury.
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