The effect of ammonia on canine polymorphonuclear cells

Area of Science:

• Veterinary Immunology
• Toxicology
• Canine Pathology

Background:

• Hyperammonaemia is a common complication in dogs with liver disease.
• High ammonia levels can cause hepatic encephalopathy (HE) and may affect the innate immune system.
• The impact of hyperammonaemia on the canine innate immune system is not well understood.

Purpose of the Study:

• To investigate the effects of ammonia on the oxidative burst activity of canine polymorphonuclear cells in vitro.
• To determine if ammonia influences spontaneous and stimulated oxidative burst responses.
• To assess the relationship between ammonia concentration and blood pH.

Main Methods:

• Blood from healthy dogs was incubated with varying ammonia concentrations (0–250 μM).
• Oxidative burst activity was measured using flow cytometry and a commercial kit (Phagoburst™).
• Measurements included spontaneous and E. coli-stimulated oxidative burst, along with blood pH.

Main Results:

• Spontaneous oxidative burst significantly increased at ammonia concentrations of 125 μM and above.
• A 4.9-fold increase in spontaneous oxidative burst was observed at 200 μM ammonia.
• No significant difference in oxidative burst was found for E. coli-stimulated cells; blood pH remained stable.

Conclusions:

• Ammonia significantly increases spontaneous oxidative burst in canine neutrophils in vitro.
• This finding suggests a potential role for ammonia in innate immune system dysfunction in dogs with liver disease.
• Modulating ammonia levels could be a future therapeutic strategy for immune dysregulation in canine liver disease.