Abscess formation causes systemic and localized up-regulation of neutrophil 
[polymorphonuclear leukocytes (PMNs)] signaling pathways. In the abscess, 
following bacterial ingestion or PMN activation by inflammatory mediators, PMN 
apoptosis is elevated and leads to the externalization of phosphatidylserine. 
Annexin-V (AnxV) has been shown to have high affinity to externalized 
phosphatidylserine. We hypothesized that (99m)Tc-AnxV will target high densities 
of apoptotic PMNs and image abscesses. AnxV, conjugated with 
hydrazinenicaotinamide (HYNIC), was labeled with reduced (99m)TcO(4)(-) and its 
purity was determined by instant thin-layer chromatography. Apoptosis was 
induced in isolated human PMNs by incubation in 2% saline for 17 and 22 h at 37 
degrees C. PMNs were then incubated with (99m)Tc-HYNIC-AnxV and associated 
(99m)Tc was determined. Abscesses were induced in mice by intramuscular 
injection of bacteria or turpentine. Following intravenous administration of 
(99m)Tc-HYNIC-AnxV, mice were imaged and tissue distribution studied at 4 and 24 
h. Radiochemical purity of (99m)Tc-HYNIC-AnxV was 84.9+/-8.11%. At 17 h, 
(99m)Tc-HYNIC-AnxV bound to apoptotic PMNs was 71.6+/-0.01% and 48.6+/-0.01% for 
experimental and control cells, respectively (P=.002). At 22 h, experimental 
cells retained 74.9+/-0.02% and control cells retained 47.2+/-0.02% (P=.005). 
(99m)Tc-HYNIC-AnxV associated with bacterial abscesses was 1.25+/-0.09 and 
3.75+/-0.83 percent injected dose per gram (%ID/g) at 4 and 24 h compared to 
turpentine abscesses which was 1.02+/-0.16 and 0.72+/-0.17 %ID/g at 4 (P<or=.05) 
and 24 h (P<or=.01). (99m)Tc-HYNIC-AnxV represents a minimally invasive and 
promising agent to image and potentially distinguish between infectious and 
inflammatory abscesses.