Early detection of oleic acid-induced lung injury in rats using In-111-labeled anti-rat intercellular adhesion molecule-1

Previous study of the bleomycin-induced lung injury model suggested that In -111-labeled antirat intercellular adhesion molecule-1 (alCAM-1) might be a useful acute respiratory distress syndrome (ARDS) diagnostic agent. We fur ther investigated the ability of In-111-alCAM-1 to detect inflammation in a nother ARDS lung injury model. Methods: In-111-labeled rat polymorphonuclea r leukocytes (PMNs), In-111-alCAM-1, In-111-labeled normal mouse IgG (nmlgG ), and In-111-labeled rat serum albumin (RSA) were injected into rats 18-24 h before kill. Biodistributions, scintigraphic images, and lung ICAM-1 upr egulation were obtained in uninjured rats and in rats after injury with ole ic acid. Results: In-111-RSA and In-111-nmlgG localized in inflamed lung at 5 min postinjury (Pl). In-111-PMN uptake increased significantly only at 2 4 h Pl. In-111-alCAM-1 localization increased significantly (30%-60%) at 1 h PI and remained elevated up to 24 h PI. Lung/blood ratios (VB) at 1 and 4 h PI were very low (<0.6) for In-111-nmlgG and In-111-PMN rats; however, f or In-111-alCAM-1 rats, they were >1 and 25%-60% higher than those for the control samples. A low VB suggests poor inflammation detection on the image s, images and region-of-interest analysis confirmed that only In-111-alCAM- 1 could distinguish inflamed lungs at 4 h PI. ICAM-1 was upregulated at 4 a nd 24 h PI. Conclusion: In this model, In-111-alCAM-1 detected lung inflamm ation Very early in the course of the disease. These results support the su ggestion that In-111-alCAM-1 could be a very early, highly specific ARDS di agnostic agent and may be useful to detect a wide range of inflammations.