The role of NOD-like receptors in the modulation of osteoclastogenesis and bone re...
| Grant number: | 14/11958-3 |
| Support type: | Scholarships in Brazil - Post-Doctorate |
| Effective date (Start): | January 01, 2015 |
| Effective date (End): | August 31, 2016 |
| Field of knowledge: | Health Sciences - Dentistry - Periodontology |
| Cooperation agreement: | Coordination of Improvement of Higher Education Personnel (CAPES) |
| Principal Investigator: | Sandra Yasuyo Fukada Alves |
| Grantee: | Erivan Schnaider Ramos Junior |
| Home Institution: | Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil |
Abstract Periodontitis is a multifactorial infectious and inflammatory chronic disease that constitutes a great challenge for researchers. One of the factors of disease severity / progression is an intense immune / inflammatory response which can lead to bone resorption triggered by the host cells in response to the complexity of bacteria and their products. Amongst these bacteria, Porphyromonas gingivalis has been a major causative agent of dysbiosis in the oral microbiota leading to disease progression. The host-pathogen interaction opens up new and interesting possibilities in the study of the immune and osseous system. In this context, the discovery of intracellular receptors (Nod1 and Nod2) which can recognize pathogens associated molecular patterns and induce an immune response has been associated with the knowledge that P. gingivalis is able to interact with such receptors, opening a new field to study. It has been demonstrated the involvement of autophagy, a new arsenal component of the innate immune system, in the production's modulation of pro-inflammatory cytokines in cells from Nod1 and Nod2 deficient mice. However, the role of these receptors in autophagic cells involved in mechanisms of bone resorption, such as macrophages and osteoclasts in the context of P. gingivalis infection remains unclear. Thus, the aim of this study is to characterize the role of autophagy caused by P. gingivalis in modulating the secretion of inflammatory mediators, cell death, damage / mitochondrial activity , ROS generation and lysosome traffic using bone marrow derived macrophages and osteoclasts ( in vitro ) of Nod1 and Nod2-deficient mice.Expected contribution to the field: provide technical / scientific information for assessing the possibility of using such information for modulating the immune response, specifically the Nod1 and Nod2 receptors, in order to give a possible clinical application as well as possibility of clinical application reaching the so-called "Translational Periodontology". It is important to emphasize that this study consists of a line of research approved by FAPESP being consistent with the work currently in development by the research group. (AU) | |
| News published in Agência FAPESP Newsletter about the scholarship: | |
| Study paves the way to a novel treatment for bone loss | |