Author(s):
Cascão, Rita 
; Moura, Rita A. ; Perpétuo, Inês ; Canhão, Helena ; Vieira-Sousa, Elsa ; Mourão, Ana F. ; Rodrigues, Ana M. ; Polido-Pereira, Joaquim ; Queiroz, Mário V. ; Rosário, Henrique S. ; Souto-Carneiro, Maria M. ; Graça, Luís ; Fonseca, João E.
Date: 2010
Persistent ID: http://hdl.handle.net/10451/6352
Origin: Repositório da Universidade de Lisboa
Subject(s): Rheumatoid arthritis; Cytokines; Neutrophil; Th17
Description
© 2010 Cascão et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Introduction: Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterized by sustained
synovitis. Recently, several studies have proposed neutrophils and Th17 cells as key players in the onset and
perpetuation of this disease. The main goal of this work was to determine whether cytokines driving neutrophil
and Th17 activation are dysregulated in very early rheumatoid arthritis patients with less than 6 weeks of disease
duration and before treatment (VERA).
Methods: Cytokines related to neutrophil and Th17 activation were quantified in the serum of VERA and
established RA patients and compared with other very early arthritis (VEA) and healthy controls. Synovial fluid (SF)
from RA and osteoarthritis (OA) patients was also analyzed.
Results: VERA patients had increased serum levels of cytokines promoting Th17 polarization (IL-1b and IL-6), as
well as IL-8 and Th17-derived cytokines (IL-17A and IL-22) known to induce neutrophil-mediated inflammation. In
established RA this pattern is more evident within the SF. Early treatment with methotrexate or corticosteroids led
to clinical improvement but without an impact on the cytokine pattern.
Conclusions: VERA patients already display increased levels of cytokines related with Th17 polarization and
neutrophil recruitment and activation, a dysregulation also found in SF of established RA. 0 Thus, our data suggest
that a cytokine-milieu favoring Th17 and neutrophil activity is an early event in RA pathogenesis.
