Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/200014
Type: Artigo de periódico
Title: 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.
Author: Silva, Juliete A F
Ferrucci, Danilo L
Peroni, Luis A
Abrahão, Patrícia G S
Salamene, Aline F
Rossa-Junior, Carlos
Carvalho, Hernandes F
Stach-Machado, Dagmar R
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-1β/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-1β (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-α 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.
Subject: Alveolar Bone Loss
Animals
Diabetes Mellitus, Experimental
Diabetes Mellitus, Type 1
Disease Progression
Gpi-linked Proteins
Gingiva
Inflammation Mediators
Interleukin-10
Interleukin-17
Interleukin-1beta
Interleukin-23
Interleukin-6
Ligation
Macrophages
Male
Matrix Metalloproteinase 13
Matrix Metalloproteinase 14
Matrix Metalloproteinase 8
Molar
Neutrophil Infiltration
Neutrophils
Periodontal Diseases
Rna, Messenger
Rats
Rats, Wistar
Th17 Cells
Time Factors
Tumor Suppressor Proteins
Up-regulation
Rights: fechado
Identifier DOI: 10.1002/jcp.22979
Address: http://www.ncbi.nlm.nih.gov/pubmed/21826658
Date Issue: 2012
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

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