Interleukin-1β, tumour necrosis factor-α and lipopolysaccharide induce C-type natriuretic peptide from canine aortic endothelial cells.

The N-terminal portion of pro C-type natriuretic peptide (NT-pCNP) has shown promise as a biomarker for sepsis in humans and dogs, however the mechanism of NT-pCNP production in dogs is unknown. Canine aortic endothelial cells were stimulated with lipopolysaccharide, lipoteichoic acid, peptidoglycan, TNF-α, IL-1β, IL-6, IL-10, IL-21, CXCL-8, IFN-γ, VEGF-A or control (PBS), and NT-pCNP production was measured. Lipopolysaccharide, TNF-α, and IL-1β significantly stimulated NT-pCNP production in a dose and time dependent manner; IL-1β resulted in the greatest NT-pCNP concentrations. The other stimulants did not result in significant NT-pCNP production. The addition of serum to the cell culture model did not alter lipopolysaccharide, lipoteichoic acid or peptidoglycan induced NT-pCNP production. These data indicate that lipopolysaccharide, TNF-α and IL-1β regulate CNP production from canine vascular endothelium and of the stimulants tested, IL-1β is the predominant inducing factor. These data provide some initial insight into the mechanisms of CNP regulation in dogs.