Early Detection of Oleic Acid-Induced Lung Injury in Rats Using 111In-Labeled Anti-Rat Intercellular Adhesion Molecule-1

Previous study of the bleomycin-induced lung injury model suggested that 111In-labeled antirat intercellular adhesion mol-ecule-1 (aICAM-1) might be a useful acute respiratory distress syndrome (ARDS) diagnostic agent. We further investigated the ability of 111In-aICAM-1 to detect inflammation in another ARDS lung injury model. Methods: 111In-labeled rat polymorphonu-clear leukocytes (PMNs), 111In-aICAM-1, 111In-labeled normal mouse IgG (nmIgG), and 111In-labeled rat serum albumin (RSA) were injected into rats 18–24 h before kill. Biodistributions, scintigraphic images, and lung ICAM-1 upregulation were ob-tained in uninjured rats and in rats after injury with oleic acid. Results: 111In-RSA and 111In-nmIgG localized in inflamed lung at 5 min postinjury (PI). 111In-PMN uptake increased significantly only at 24 h PI. 111In-aICAM-1 localization increased significantly (30%–60%) at 1 h PI and remained elevated up to 24 h PI. Lung/blood ratios (L/B) at 1 and 4 h PI were very low (,0.6) for 111In-nmIgG and 111In-PMN rats; however, for 111In-aICAM-1 rats, they were.1 and 25%–60 % higher than those for the control samples. A low L/B suggests poor inflammation detec-tion on the images. Images and region-of-interest analysis con-firmed that only 111In-aICAM-1 could distinguish inflamed lungs at 4 h PI. ICAM-1 was upregulated at 4 and 24 h PI. Conclusion: In this model, 111In-aICAM-1 detected lung inflammation very early in the course of the disease. These results support the suggestion that 111In-aICAM-1 could be a very early, highly specific ARDS diagnostic agent and may be useful to detect a wide range of inflammations. Key Words: inflammation; acute respiratory distress syndrome; adhesion molecules; inflammation imaging; immunoscintigraph