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Publication : Inflammation is more persistent in type 1 diabetic mice.

First Author  Graves DT Year  2005
Journal  J Dent Res Volume  84
Issue  4 Pages  324-8
PubMed ID  15790737 Mgi Jnum  J:112485
Mgi Id  MGI:3656409 Doi  10.1177/154405910508400406
Citation  Graves DT, et al. (2005) Inflammation is more persistent in type 1 diabetic mice. J Dent Res 84(4):324-8
abstractText  Whether diabetes enhances or diminishes the host response to bacteria has been controversial. To determine how diabetes alters the inflammatory response, we inoculated P. gingivalis into the scalps of mice rendered diabetic with multiple low-dose streptozotocin treatment. On day 1, a moderate to severe inflammatory infiltrate was noted in both the diabetic and normoglycemic mice. After 3 days, the inflammatory infiltrate was significantly higher in the diabetic compared with the control group (P < 0.05). The mRNA expression of chemokines macrophage inflammatory protein-2 and monocyte chemoattractant protein-1 was strongly and similarly induced 3 hrs and 1 day post-inoculation. By day 3, the levels were reduced in normoglycemic mice but remained significantly higher in the diabetic group (P < 0.05). To determine whether persistent inflammation was specific for the streptozotocin-induced diabetic model, we directly compared the expression of TNF-alpha in streptozotocin-induced and db/db diabetic mice, which developed type 2 diabetes. Both exhibited prolonged TNF-alpha expression compared with controls. These results suggest that diabetes alters bacteria-host interactions by prolonging the inflammatory response.
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