| Grant number: | 17/07162-7 |
| Support Opportunities: | Scholarships in Brazil - Doctorate |
| Start date: | October 01, 2017 |
| End date: | April 30, 2021 |
| Field of knowledge: | Biological Sciences - Physiology |
| Principal Investigator: | Carlos Amilcar Parada |
| Grantee: | Nathalia Santos Carvalho |
| Host Institution: | Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil |
Abstract Rheumatoid Arthritis (RA) is an autoimmune, systemic and chronic disease of inflammatory origin that affects mainly the lining of the joints and its structures and other connective tissues, dramatically impacting the patient's quality of life and, although the contribution of genetic and environmental factors to disease development are well known, those driving to autoimmunity remains unclear. Beyond swelling, the joint pain is described as the major issue to AR patients, being the main factor that drives to disability. The inflammation and joint damage in this pathology result from a massive cell infiltrate from it 90% corresponds to neutrophils, suggesting a casual role of these cells to AR development. Additionally, the inhibition of prostanoid synthesis by Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) reliefs both, the inflammation and pain, being clinically employed as the first-choice treatment of the AR symptoms, even presenting serious adverse effects. Aiming to avoid such effects, this project wishes to employ an experimental model of Collagen Induced AR (CIA) in mice lacking COX-2 gene specifically in neutrophils, aiming to investigate whether neutrophil-released prostanoids play a key role on the initiation and development of inflammation and hyperalgesia during experimental AR. (AU) | |
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