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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Sequential IL-23 and IL-17 and increased Mmp8 and Mmp14 expression characterize the progression of an experimental model of periodontal disease in type 1 diabetes

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Author(s):
Silva, Juliete A. F. [1] ; Ferrucci, Danilo L. [1] ; Peroni, Luis A. [1] ; Abrahao, Patricia G. S. [1] ; Salamene, Aline F. [1] ; Rossa-Junior, Carlos [2] ; Carvalho, Hernandes F. [1, 3] ; Stach-Machado, Dagmar R. [1]
Total Authors: 8
Affiliation:
[1] State Univ Campinas UNICAMP, Dept Anat Cell Biol Physiol & Biophys, Campinas, SP - Brazil
[2] Araraquara UNESP, Sch Dent, Dept Diag & Surg, Sao Paulo - Brazil
[3] Natl Inst Sci & Technol Photon Appl Cell Biol INF, Campinas, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Journal of Cellular Physiology; v. 227, n. 6, p. 2441-2450, JUN 2012.
Web of Science Citations: 22
Abstract

Molecular mechanisms responsible for periodontal disease (PD) and its worsening in type 1 Diabetes Mellitus (DM1) remain unknown. Cytokine profile and expression levels of collagenases, Mmp14, and tissue inhibitors were determined, as were the numbers of neutrophils and macrophages in combined streptozotocin-induced DM1 and ligature-induced PD models. Increased IL-23 (80-fold) and Mmp8 expression (25-fold) was found in DM1. Ligature resulted in an IL-1 beta/IL-6 profile, increased expression of Mmp8, Mmp13, and Mmp14 (but not Mmp1), and transient expression of Timp1 and Reck in non-diabetics. PD in DM1 involved IL-1 beta (but not IL-6) and IL-23/IL-17, reduced IL-6 and IL-10, sustained Mmp8 and Mmp14, increased Mmp13 and reduced Reck expression in association with 20-fold higher counts of neutrophils and macrophages. IL-23 and Mmp8 expression are hallmarks of DM1. In association with the IL-1/IL-6 (Th1) response in PD, one found a secondary IL-17 (Th17) pathway in non-diabetic rats. Low IL-6/TNF-a suggest that the Th1 response was compromised in DM1, while IL-17 indicates a prevalence of the Th17 pathway, resulting in high neutrophil recruitment. Mmp8, Mmp13, and Mmp14 expression seems important in the tissue destruction during PD in DM1. PD-associated IL-1/IL-6 (Th1), IL-10, and Reck expression are associated with the acute-to-chronic inflammation transition, which is lost in DM1. In conclusion, IL-23/IL-17 are associated with the PD progression in DM1. J. Cell. Physiol. 227: 24412450, 2012. (c) 2011 Wiley Periodicals, Inc. (AU)