This study was undertaken to evaluate whether Tc-99m-labeled human neutroph
il peptide (HNP)-1 can be used as a tracer for rapid visualization of bacte
rial infections. Methods: Mice were injected intramuscularly with 1 million
Staphylococcus aureus or Klebsiella pneumoniae organisms and 5 min later w
ere injected intravenously with 0.4 mu g (0.8 MBq) Tc-99m-HNP-1. At various
intervals, detailed information about clearance and accumulation of this t
racer at sites of infection and in various organs was obtained by scintigra
phy. Tc-99m-labeled immunoglobulin G (IgG), an established marker of infect
ion and inflammation, was used for comparison. Results: After injection int
o S. aureus- or K. pneumoniae-injected mice, Tc-99m-HNP-1 was rapidly remov
ed from the circulation, mainly th rough the kidneys and bladder, with half
-fives of 170 and 55 min, respectively. Similar half-lives were observed fo
r Tc-99m-IgG in these animals. Visualization of foci with S. aureus or K. p
neumoniae, as indicated by a ratio of 1.3 or higher between the targeted th
igh muscle (containing bacteria) and the nontargeted (contralateral) thigh
muscle (TINT), was already achieved 5 min after injection of Tc-99m-HNP-1.
Similar T/NTs for Tc-99m-IgG were obtained 4 h after injection of the trace
r, indicating that imaging of foci of bacteria with Tc-99m-HNP-1 is much fa
ster than with Tc-99m-IgG. To Obtain insight into factors that contribute t
o accumulation of Tc-99m-HNP-1 at sites of infection, the binding of this t
racer to bacteria and leukocytes was assessed using a peritoneal infection
model. Binding of Tc-99m-HNP-1 to bacteria was approximately 1000 times hig
her than binding to leukocytes. Although the number or bacteria in the peri
toneum was 1000-fold lower than the number of leukocytes, a significant cor
relation between binding or Tc-99m-HNP-1 to bacteria on the one hand and ac
cumulation of tracer on the other was still found, in contrast to Tc-99m-Ig
G. Conclusion: Tc-99m-HNP-1 allows rapid visualization or bacterial infecti
ons. Binding of this tracer to bacteria most likely contributes significant
ly to the accumulation of Tc-99m-HNP-1 at sites of infection.