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Evaluation of the respiratory burst induced by receptors Fc R and CR was carried out in peripheral blood neutrophils (PBN) in rheumatoid arthritis (RA) patients with active and inactive disease. Simultaneously, cooperation between these receptors and their expression, PBN chemotaxis, and complement system systemic activity were also investigated. Neutrophils were stimulated with IC-IgG opsonized with normal human serum (NHS) or not, or with IC-IgG opsonized with RA human serum (RAHS). ROS production was increased in neutrophils of patients with active or inactive RA stimulated of IC-IgG opsonized with NHS compared to the response of the cells mediated by ICIgG. However, there was poor Fc R/CR cooperation in these RA neutrophils, as indicated by decreased ROS production upon stimulation with IC-IgG opsonized with RAHS. In the case of active RA patients, neutrophils presented significantly higher CR1 and CR3 expression, as well as slight elevation in CD32 and CD16 expression. Positive correlations between Fc R and CR, complement alternative pathway activation, and increased RA serum chemotaxic activity were only detected in active RA patients. Taken together, these results indicate that several abnormalities of the complement system exist at the systemic level, namely impaired membrane receptor cooperation, alternative pathway activation, and presence of pre-existing chemoattractant factors in the serum, as reflected by the neutrophil function in the particular case of active RA patients. All, these abnormalities may synergistically contribute to RA pathogenesis.

Rheumatoid arthritis (RA) is a highly disabling disease that affects all structures of the joint and significantly impacts on morbidity and mortality in RA patients. RA is characterized by persistent inflammation of the synovial membrane lining the joint associated with infiltration of immune cells. Eighty to 90% of the leukocytes infiltrating the synovia are neutrophils. The specific role that neutrophils play in the onset of RA is not clear, but recent studies have evidenced that they have an important participation in joint damage and disease progression through the release of proteolytic enzymes, reactive oxygen species (ROS), cytokines, and neutrophil extracellular traps, in particular during frustrated phagocytosis of immune complexes (ICs). In addition, the local and systemic activation of the complement system contributes to the pathogenesis of RA and other IC-mediated diseases. This review discusses (i) the participation of Fcγ and complement receptors in mediating the effector functions of neutrophils in RA; (ii) the contribution of the complement system and ROS-dependent and ROS-independent mechanisms to joint damage in RA; and (iii) the use of plant extracts, dietary compounds, and isolated natural compounds in the treatment of RA, focusing on modulation of the effector functions of neutrophils and the complement system activity and/or activation.

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