LAUSR

Background People with critical illness (CI) commonly develop various forms of immune dysfunction, however, there is limited information concerning immune dysfunction in dogs with CI. Hypothesis The immune response in CI dogs differs from that of healthy dogs. Animals Immunologic variables were compared between 14 dogs with CI, defined as APPLEfast score of >20 points, admitted to the University of Missouri Veterinary Health Center Small Animal Clinic Intensive Care Unit and healthy controls (n = 15). Methods Cohort study evaluating constitutive and lipopolysaccharide (LPS)‐stimulated TNF‐α, IL‐6, and IL‐10 production, phagocytosis of opsonized E. coli and respiratory burst capacity after opsonized E. coli or phorbol 12‐myristate 13‐acetate (PMA) stimulation, peripheral blood lymphocyte phenotype, and monocyte expressions of HLA‐DR and TLR‐4. Results Lipopolysaccharide‐stimulated leukocyte TNF‐α (median, Q1, Q3; CI, 49, 49, 120; control, 655, 446, 1174 pg/mL; P = < 0.001), IL‐6 (median, Q1, Q3; CI, 49, 49, 64; control, 100, 49, 166 pg/mL; P = 0.029), and IL‐10 (CI, 49, 49, 56; control, 96, 49, 203 pg/mL; P = 0.014) production and both E. coli (median, Q1, Q3; CI, 60.5, 43, 88.5; control, 86.6, 81, 89.2%; P = 0.047) and PMA (CI, 40, 11.7, 70; control, 93, 83, 97.6%; P = < 0.001)‐stimulated respiratory burst capacity significantly decreased in CI dogs. Percentage of monocytes expressing TLR‐4 greater in the CI dogs (median, Q1, Q3; CI, 46.9, 24.3, 64.2; control, 16.4, 9.4, 26.2%; P = 0.005). Conclusion These findings suggest dogs with CI develop immune system alterations that result in reduced respiratory burst function and cytokine production despite upregulation of TLR‐4.