Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Click here to sign up for SAGE Journal Email Alerts today!

Sign In to gain access to subscriptions and/or personal tools.
Journal of Dental Research
This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Graves, D.T.
Right arrow Articles by Krall, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Graves, D.T.
Right arrow Articles by Krall, E.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Biological

Inflammation is More Persistent in Type 1 Diabetic Mice

D.T. Graves*, G. Naguib, H. Lu, C. Leone, H. Hsue and E. Krall

Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Suite W-202D, 700 Albany Street, Boston, MA 02118, USA;

Correspondence: * corresponding author, dgraves{at}bu.edu

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.

Key Words: cytokine • hyperglycemia • inflammation • leukocyte • MIP-2 • MCP-1 • TNF-{alpha} • PMN • periodontal

Journal of Dental Research, Vol. 84, No. 4, 324-328 (2005)
DOI: 10.1177/154405910508400406
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
Q. Zhou, S. E. Leeman, and S. Amar
Signaling mechanisms involved in altered function of macrophages from diet-induced obese mice affect immune responses
PNAS, June 30, 2009; 106(26): 10740 - 10745.
[Abstract] [Full Text] [PDF]