From scRNA-seq to therapeutic targets: Unveiling the impact of activated mast cells on intestinal dysfunction in acute pancreatitis

Table 1 Key outcome summary

Key outcome	Observation in AP small intestine	Implication
Intestinal cellular heterogeneity	scRNA-seq of the small intestine identified 17 distinct cell clusters from > 33000 cells across the control, AP1, and AP2 samples	Provides a high-resolution atlas of the small-intestinal cell composition and reveals dynamic shifts during early AP
Intestinal MC activation	scRNA-seq showed an apparent reduction of MC recovery but immunofluorescence staining (c-Kit and toluidine blue) confirmed stable MC counts with degranulation	Highlights activation-induced MC fragility during dissociation and underscores MC mediator release as a driver of barrier dysfunction
CCL5 upregulation in intestinal MCs	scRNA-seq and flow cytometry demonstrated significant CCL5 overexpression in MCs in the AP1 and AP2 groups	Identifies CCL5 as a key chemokine, mediating neutrophil and macrophage recruitment to the gut barrier
Tight junction disruption in small intestine	IHC revealed decreased expression of ZO-1 and occludin in AP1 and AP2 intestinal epithelia	Confirms compromised epithelial barrier integrity at early stages of AP
Programmed cell death in enterocytes	IHC showed increase in cleaved caspase-3 (apoptosis) and p-MLKL (necroptosis) levels in intestinal enterocytes from the control to AP1 to AP2 group	Demonstrates enterocyte loss via multiple cell-death pathways contributing to barrier breakdown

AP: Acute pancreatitis; MC: Mast cell; IHC: Immunohistochemistry.