Journal of equine veterinary science · 2026
Downregulation of a choline transporter gene in equine colitis indicates a role for choline supplementation to support the large intestinal epithelial barrier.
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Sheahan B J, O'Neill M K, Jeter M A, McDermott L B, Megeed H S
Аннотация
BACKGROUND: Acute colitis is an inflammatory condition of the equine colon associated with high morbidity and mortality. In these horses, epithelial barrier function is critical but the mechanisms underlying large intestinal epithelial damage and recovery are incompletely understood.
AIMS/OBJECTIVES: Our objectives were to (1) identify intestinal colitis-associated transcriptional pathways, and (2) determine the effect of in vitro choline supplementation on the epithelial barrier.
METHODS: We performed RNA-sequencing on rectal biopsies from healthy and colitis horses (n = 3/group). Downregulated SLC5A7, a gene encoding CHT1 (High-Affinity Choline Transporter 1), was confirmed using qRT-PCR and immunofluorescence on large intestinal (cecum, right ventral colon (RVC), right dorsal colon (RDC), and rectum) biopsies from additional healthy and colitis horses (n = 8-20/group). Primary monolayer epithelial cultures derived from healthy RDC (n = 4 horses) were treated with 0-250 µM choline and monitored for cellular proliferation and barrier permeability.
RESULTS: We identified a colitis-associated transcriptome in rectal biopsies, including upregulated inflammatory response, cell cycle, and epithelial reorganization gene sets. There was decreased SLC5A7 expression throughout large intestinal biopsies of colitis horses (healthy cecum mean log2 fold change 1.8, 95% CI [1.12, 2.67] vs colitis cecum mean log2 fold change -0.5, 95% CI [-1.42, 0.42]). Apical epithelial CHT1 immunofluorescence was diminished in cecum, RVC, and RDC biopsies from colitis horses. Choline supplementation increased cellular proliferation and decreased time to confluency of epithelial monolayers, however no difference in barrier permeability post-confluency was observed.
CONCLUSION: Acute equine colitis has a distinct transcriptomic signature. Our findings suggest that choline supplementation may encourage epithelial barrier recovery.
AIMS/OBJECTIVES: Our objectives were to (1) identify intestinal colitis-associated transcriptional pathways, and (2) determine the effect of in vitro choline supplementation on the epithelial barrier.
METHODS: We performed RNA-sequencing on rectal biopsies from healthy and colitis horses (n = 3/group). Downregulated SLC5A7, a gene encoding CHT1 (High-Affinity Choline Transporter 1), was confirmed using qRT-PCR and immunofluorescence on large intestinal (cecum, right ventral colon (RVC), right dorsal colon (RDC), and rectum) biopsies from additional healthy and colitis horses (n = 8-20/group). Primary monolayer epithelial cultures derived from healthy RDC (n = 4 horses) were treated with 0-250 µM choline and monitored for cellular proliferation and barrier permeability.
RESULTS: We identified a colitis-associated transcriptome in rectal biopsies, including upregulated inflammatory response, cell cycle, and epithelial reorganization gene sets. There was decreased SLC5A7 expression throughout large intestinal biopsies of colitis horses (healthy cecum mean log2 fold change 1.8, 95% CI [1.12, 2.67] vs colitis cecum mean log2 fold change -0.5, 95% CI [-1.42, 0.42]). Apical epithelial CHT1 immunofluorescence was diminished in cecum, RVC, and RDC biopsies from colitis horses. Choline supplementation increased cellular proliferation and decreased time to confluency of epithelial monolayers, however no difference in barrier permeability post-confluency was observed.
CONCLUSION: Acute equine colitis has a distinct transcriptomic signature. Our findings suggest that choline supplementation may encourage epithelial barrier recovery.