CD‐14 expression in hepatic tissue of horses with laminitis

Abstract

Researchers hypothesize that laminitis in horses, due to introduction of bacterial components (i.e. endotoxins) into the systemic circulation from GI disturbance, signal an innate immune/inflammatory response via the Toll‐Like Receptor (TLR) Signaling Pathway. TLR‐4 is predominantly responsible for the response to G‐ bacteria and we found this gene was upregulated 3‐fold in laminitic horses compared to controls. The co‐receptor, Cluster of Differentiation 14 (CD‐14), transports endotoxins TLR‐4. We hypothesize that upregulation of TLR‐4 may correlate with expression of CD‐14.Equine CD‐14 expression was measured using TaqMan RT‐PCR in liver samples from normal, cases with metabolic disease, and those with naturally acquired or experimentally‐induced laminitis. The primers and probe for equine CD‐14 were designed from the NCBI published equine CD‐14 gene sequences (AF200416, NM 001081927). Data is expressed as ΔΔCT (Critical Temperature units).CD‐14 decreased 0.3561 fold from that of normal horses. Horses with metabolic predispositions for laminitis had a 9.8758 fold increase in CD‐14 expression. Decreased CD‐14 in laminitic horses may not directly correlate with TLR‐4 up‐regulation; therefore more studies need to be performed to understand the potential role of CD‐14 as it relates to laminitis pathogenesis. Funding by the LSU Equine Health Studies Program.