Rotating Equine Intern North Carolina State University Raleigh, North Carolina
Investigating the Use of a Novel Amnion Product to Enhance Intestinal Repair in Horses. Veerasammy B, Bayless R, Sheats MK, Gonzalez L. North Carolina State University, Raleigh, NC.
Horses with severe intestinal disease experience intestinal hypoxia and inflammation which contribute to intestinal barrier breakdown. The compromised barrier can lead to systemic inflammatory response syndrome. Treatment currently involves anti-inflammatory and anti-endotoxin therapies to sustain horses during intestinal epithelial repair. Reports suggest accelerated epithelial wound healing in skin with a novel acellular amnion product. This product enhances healing by establishing an extracellular matrix, providing growth factors, and exerting local anti-inflammatory effects. However, it is unknown whether acellular amnion could enhance healing and/or suppress inflammation in injured intestinal epithelium. We hypothesize that acellular amnion will hasten repair of hypoxia-induced small intestinal epithelial injury, ex vivo, and will attenuate neutrophilic migration, in vitro. Banked samples of intestinal epithelial stem cells derived from donated horses euthanized for reasons unrelated to colic were used to create monolayers. Ex vivo injury was induced by subjecting confluent monolayers to four hours of 1% hypoxia, followed by creation of a linear defect. Epithelial barrier repair was determined by measuring the time to defect closure. Equine neutrophils were isolated from healthy living donor venous blood and chemotaxis was evaluated. Treatment groups included acellular amnion, vehicle and untreated controls. Monolayers were treated postinjury and neutrophils were treated prior to chemotaxis assays (n = 2). 80% closure was achieved in the amnion treated monolayer compared to control (34%) at sixteen hours post scratch assay. Acellular amnion decreased percent of neutrophil migration (29.45 ± 12.66) compared to control (74.25 ± 8.42). Preliminary data supports the potential of acellular amnion to hasten epithelial repair and attenuate neutrophil migration.