Abstract 15950: Development of Near-Infrared Nanoprobes for in vivo Monitoring of Fibrin Deposition and Inflammatory Responses
Objective Fibrin deposition has been shown to accelerate vascular and lung inflammation. It is thus believed that the extent of fibrin accumulation determines the degree of inflammatory reactions in tissue. To test this hypothesis, fibrin-affinity nanoprobes (FNPs) were fabricated and then tested for their ability to detect and quantify both fibrin deposition and inflammatory responses in vivo.
Methods FNPs were produced by conjugating fibrin affinity peptide (Gly-Pro-Arg-Pro-Pro) with near infrared dye-labeled nanoprobes. The ability of FNPs to detect fibrin deposition and inflammatory responses were evaluated using various in vivo models.
Results We first assessed the efficacy of FNPs to detect fibrin deposition in vivo using polyethylene terephthalate (PET) disks-precoated with either fibrin or albumin. After being implanted subcutaneously with various treated PET disks for 24 hours, Balb/C mice were intravenously administered with FNPs. Within 2 hours of FNP administration, using a Kodak in Vivo FX imaging system, strong fluorescence was found to be associated with fibrin-coated, but not albumin-coated disk (Fig 1a). In a separate study, mice were injected with LPS to induce subcutaneous inflammation for 24 hours prior to FNPs injection. As expected, the fluorescence intensities of the LPS injection sites were significantly higher than the saline sites at all time points (Fig 1b). The average fluorescence intensities in LPS-site are ~6 folds higher than saline-controls at the 24-hour time point (Fig. 1c). In support of our hypothesis, histological analyses also revealed that, at 24 hours, the tissues surrounding the LPS accumulated significantly more (~8 folds) inflammatory cells than the saline injection site (Fig 1d).
Conclusion The results support that FNPs and fluorescence imaging technique may serve as a powerful tool to continuously monitor and quantify the extent of fibrin deposition and associated inflammatory responses in vivo.
- © 2011 by American Heart Association, Inc.