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111 In‐DANBIRT as An in Vivo SPECT/CT Imaging Tool for The Expression of LFA‐1 in The Inflammatory Process of Atheroma Development
Author(s) -
Mota Roberto Ivan,
Daniels Tamara,
Nysus Monique,
Lucas Selita,
Norenberg Jeffrey,
Campen Matthew
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1177.22
Subject(s) - medicine , aortic arch , atheroma , in vivo , pathology , aorta , lesion , immune system , nuclear medicine , immunology , biology , microbiology and biotechnology
Objective Assess inflammatory leukocyte presence and accumulation in vascular atherosclerotic plaque using 111 In‐DANBIRT as a non‐invasive diagnostic imaging tool. Methods 6 week ApoE KO mice were fed either normal or high fat chow (n=8 per group) for 8 weeks to induce vascular atherosclerotic lesions. SPECT/CT imaging was performed 3 hours post injection of ~700uCi of 111 In‐DANBIRT at baseline, 4 weeks and 8 weeks. Whole body Autoradiography was performed 24 hours post injection after the 8 week time point. Image processing and analysis was performed by region of interest (ROI) determination in relationship to voxel and volume, uptake quantification was normalized to muscle uptake. Blood partition assays were conducted to ascertain specific binding components. Results Autoradiography and SPECT/CT analysis characterized 111 In‐DANBIRT distribution in cardiovascular tissues (heart, aortic arch, descending aorta, carotids). A longitudinal increase in uptake was evidenced when comparing high fat diet to normal diet mice along our different time points. Increased uptake was evidenced in the thymus, which would be consistent with increased immune response to vascular injury. Whole blood isolation correlated these findings showing increased specific uptake by neutrophils in our ozone‐exposed group. Conclusions This pilot study showed that ApoE KO mice on Western diet exhibit increased cardiovascular and immune tissue uptake of 111 In‐DANBIRT compared to mice on a normal diet. We still need to assess vascular lesion development in our disease model using biochemical markers and histology. Findings support future investigation of a more advanced vascular disease model that will validate 111 In‐DANBIRT as a diagnostic tool for assessment of inflammation in cardiovascular injury models. Support or Funding Information Data was generated in the Keck‐UNM Small‐Animal Imaging Resource Shared Resource Center supported by the University of New Mexico Health Sciences Center, the UNM Cancer Center, and UNM College of Pharmacy. Grant numbers: NIH P30CA118100‐06 & ES0014639.