title: Inflammation is more persistent in type 1 diabetic mice.
abstract: 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.
authors.affiliation: Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Suite W-202D, Boston, MA 02118, USA. dgraves@bu.edu
authors.forename: D T
authors.initials: DT
authors.lastname: Graves
authors.forename: G
authors.initials: G
authors.lastname: Naguib
authors.forename: H
authors.initials: H
authors.lastname: Lu
authors.forename: C
authors.initials: C
authors.lastname: Leone
authors.forename: H
authors.initials: H
authors.lastname: Hsue
authors.forename: E
authors.initials: E
authors.lastname: Krall
mesh_terms: D000818:Animals; D018932:Chemokine CCL2 / Q000096:biosynthesis; D054426:Chemokine CXCL2; D018925:Chemokines / Q000096:biosynthesis*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology*; D007249:Inflammation / Q000378:metabolism / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D015846:Monokines / Q000096:biosynthesis; D018375:Neutrophil Activation; D016966:Porphyromonas gingivalis / Q000472:pathogenicity; D013311:Streptozocin; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D018932:Chemokine CCL2; D054426:Chemokine CXCL2; D018925:Chemokines; D015846:Monokines; D014409:Tumor Necrosis Factor-alpha; D013311:Streptozocin