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Acta Physiologica 2009; Volume 196, Supplement 671
Scandinavian Physiological Society’s Annual Meeting
8/14/2009-8/16/2009
Uppsala, Sweden
LEUKOCYTE RECRUITMENT IN RESPONSE TO MIP-2 IN DIABETIC MICE
Abstract number: O18
PETTERSSON1 U, HENRIKSNAS1 J, JANSSON1 L, PHILLIPSON1 M
1Uppsala University, Dept of Medical Cell Biology, Box 571, Husargatan 3, 75123, Uppsala, Sweden. [email protected]
Objective:
Diabetes is associated with a general sub- clinical inflammation, the origin of which is uncertain. The aim of this study was to evaluate if high blood glucose concentrations influenced leukocyte recruitment in an established model of inflammation. Methods: Intravital microscopy was used to study leukocyte recruitment in venules (~35mm in diameter) in the cremaster muscle of anaesthetized control and hyperglycemic C57Bl/6 mice. Hyperglycemia was induced by i.v. administration of alloxan, a b-cell toxin, 3 days prior intravital experiment (75 mg/kg b.w, Sigma-aldrich, UK). Blood flow was recorded in 5- minute periods at time points 0, 30, 60, and 90 minutes, where after rolling velocity and the number of rolling, adherent and emigrated leukocytes were quantified. Superfusion of MIP-2 (a chemokine, 0.5 nM, R&D systems, UK) was initiated after the first recording period and then continued throughout the experiment.
Results:
At the day of experiment, blood glucose levels were 9.6 and >28 mmol/l in control and alloxan- diabetic mice respectively. MIP-2 superfusion resulted in decreased rolling velocity and number of rolling cells, in addition to increased number of adherent and emigrated leukocytes in control mice. Similar numbers of rolling and adherent leukocytes were seen in the diabetic mice both at time point 0 and after MIP- 2 activation. However, the number of emigrated cells was significantly increased in diabetic mice compared to controls at time 0 as well as after MIP-2 activation.
Conclusion:
The number of emigrated leukocytes was increased in diabetic mice, which might depend on amplified endothelial activation by the hyperglycemia.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 196, Supplement 671 :O18