Chemotactic peptide uptake in acute pancreatitis: correlation with tissue accumulation of leukocytes

Citation
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
Citations number
26
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Physiology
Journal title
JOURNAL OF APPLIED PHYSIOLOGY
ISSN journal
8750-7587 → ACNP
Volume
87
Issue
2
Year of publication
1999
Pages
743 - 749
Database
ISI
SICI code
8750-7587(199908)87:2<743:CPUIAP>2.0.ZU;2-J
Abstract
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.