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Contribution of COX-2 expression of neutrophils in the inflammatory process and in hyperalgesia during experimental Rheumatoid Arthritis induced by collagen in mice

Grant number: 17/07162-7
Support type:Scholarships in Brazil - Doctorate
Effective date (Start): October 01, 2017
Effective date (End): February 29, 2020
Field of knowledge:Biological Sciences - Physiology
Principal Investigator:Carlos Amilcar Parada
Grantee:Nathalia Santos Carvalho
Home 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)