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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

Processo: 12/03833-0
Linha de fomento:Auxílio à Pesquisa - Publicações científicas - Artigo
Vigência: 01 de abril de 2012 - 30 de setembro de 2012
Área do conhecimento:Ciências Biológicas - Imunologia - Imunologia Celular
Pesquisador responsável:Dagmar Ruth Stach - Machado
Beneficiário:Dagmar Ruth Stach - Machado
Instituição-sede: Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brasil


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 neutrophilsand macrophages in combined streptozotocin-induced DM1 and ligature-induced PD models. Increased IL-23 (80-fold) and Mmp8expression (25-fold) was found in DM1. Ligature resulted in an IL-1b/IL-6 profile, increased expression ofMmp8, Mmp13, and Mmp14 (butnot Mmp1), and transient expression of Timp1 and Reck in non-diabetics. PD inDM1involved IL-1b (but not IL-6) and IL-23/IL-17, reducedIL-6 and IL-10, sustained Mmp8 and Mmp14, increased Mmp13 and reduced Reck expression in association with 20-fold higher counts ofneutrophils 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 inDM1, while IL-17 indicates a prevalence of the Th17 pathway, resulting in high neutrophil recruitment. Mmp8, Mmp13, and Mmp14expression seems important in the tissue destruction during PD in DM1. PD-associated IL-1/IL-6 (Th1), IL-10, and Reck expression areassociated with the acute-to-chronic inflammation transition, which is lost in DM1. In conclusion, IL-23/IL-17 are associated with the PDprogression in DM1. (AU)