W. Hartwig et al., Chemotactic peptide uptake in acute pancreatitis: correlation with tissue accumulation of leukocytes, J APP PHYSL, 87(2), 1999, pp. 743-749
Chemotactic peptides bind specifically to receptors on leukocyte membranes.
This property makes them prospective vehicles to evaluate inflammation and
infection. We used two well-established models of acute pancreatitis to qu
antitate the binding of the chemotactic peptide N-formyl-methionyl-leucyl-p
henylalanine-lysine (fMLFK) to leukocytes and its correlation to degree of
organ inflammation. Uptake of the Tc-99m-labeled nicotinyl hydrazine-deriva
tized chemotactic peptide analog fMLFK-HYNIC was measured in blood, pancrea
s, lung, and muscle specimens in rats with edematous or necrotizing pancrea
titis and was compared with neutrophil sequestration assessed by myeloperox
idase activity and histology. Chemotactic peptide uptake in the pancreas wa
s increased in mild and severe pancreatitis compared with controls, with hi
gher levels in severe than in mild disease, and correlated with tissue myel
operoxidase activity (r = 0.7395, P < 0.001). Increased pulmonary uptake on
ly in severe pancreatitis reflected pancreatitis-induced neutrophil sequest
ration in the lungs. Muscle uptake was unchanged compared with controls. Ed
ema formation did not affect chemotactic peptide uptake. The data suggest t
hat uptake of chemotactic peptides can contribute to quantitative assessmen
t of neutrophils in localized inflammatory processes and is independent of
associated edema formation or microcirculatory compromise.