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Shouval, D.

Publications and source records attributed to Shouval, D..

2 recordsLinked to original sources

Spatial Rewiring of Enterocyte Identity in Celiac Disease

Enterocytes in the human small intestine exhibit distinct functional states in different zones along the crypt-villus axis, a feature that is thought to convey optimal absorption. In celiac disease (CeD), autoimmune destruction of enterocytes leads to villus blunting, but how this altered tissue morphology affects enterocyte states is unclear. Using spatial and single-cell transcriptomics, we show that in patients with CeD, enterocytes acquire a novel identity characterized by co-expression of multiple zonal programs. This aberrant zonal co-expression results from reduced distances between BMP- and WNT-producing mesenchymal cells, leading to overlapping morphogen fields. In addition, we identify a subset of metaplastic cells that adopt gastric pit cell-like identities in discrete tissue patches. Our findings provide a detailed view of epithelial remodeling in CeD and establish a resource for understanding the cellular basis of malabsorption associated with villus blunting.

systems biology↗

Single cell atlas of the neonatal small intestine with necrotizing enterocolitis

Necrotizing enterocolitis (NEC) is a gastrointestinal complication of premature infants with high rates of morbidity and mortality. A comprehensive view of the cellular changes and aberrant interactions that underlie this disease is lacking. Here, we combine single cell RNA sequencing, T Cell Receptor beta (TCR{beta}) analysis, bulk transcriptomics, and imaging to characterize cell identities, interactions and zonal changes in NEC. We find that inflammatory macrophages are abundant in NEC and that T cells exhibit increased expression of inflammatory genes and cytokines accompanied by an increase in TCR{beta} clonal expansion. Fibroblasts and endothelial cells increase in proportion and exhibit a switch to an activated pro-inflammatory state. Villus tip epithelial cell identity is substantially reduced in NEC and the remaining epithelial cells up-regulate pro-inflammatory genes. We establish a detailed map of aberrant epithelial-mesenchymal-immune interactions that may be driving inflammation in NEC mucosa. Our analyses highlight the cellular changes underlying NEC disease pathogenesis and identify potential targets for biomarker discovery and therapeutics.

immunology↗