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2015 ; 16
(ä): 159
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Enhanced neutrophil phagocytic capacity in rheumatoid arthritis related to the
autoantibodies rheumatoid factor and anti-cyclic citrullinated peptides
#MMPMID26123215
de Siqueira MB
; da Mota LM
; Couto SC
; Muniz-Junqueira MI
BMC Musculoskelet Disord
2015[Jun]; 16
(ä): 159
PMID26123215
show ga
BACKGROUND: There is no consensus on the mechanisms by which anti-cyclic
citrullinated peptide antibodies (anti-CCP) and rheumatoid factor (RF) influence
the pathogenesis of rheumatoid arthritis (RA). The current study verified if the
presence of RF or anti-CCP is associated with phagocytic capacity and reactive
oxygen species (ROS) production by phagocytes in RA patients to better clarify
the role played by these antibodies in pathogenesis of the disease. METHODS: A
cohort of 30 RA patients followed from early stages of the disease were
characterized by positivity for RF or anti-CCP, disease activity score (DAS-28),
health assessment questionnaire (HAQ), use of synthetic or biologic therapy,
lifestyle, comorbidities and radiographic erosions. Phagocytic capacity against
Saccharomyces cerevisiae and superoxide anion production were assessed in RA
patients and compared with 20 healthy controls. Phagocytic capacity and
superoxide anion production were also compared between RF- and anti-CCP-positive
and -negative RA patients. RESULTS: Anti-CCP- and RF-positive RA patients had
higher neutrophil phagocytic capacity than anti-CCP- (p?=?0.005) and RF
(p?=?0.005)-negative individuals through pattern-recognition receptors. As
assessed via pattern recognition or opsonin receptors, neutrophils and monocytes
from RA patients presented overall higher phagocytic capacity than neutrophils
and monocytes from healthy controls (p?0.05). Furthermore, RA patients also
showed a higher capacity for producing cytotoxic oxygen radicals (p?=?0.0026).
Phagocytosis and superoxide anion production did not correlate with any of the
clinical variables analyzed in this study. CONCLUSIONS: This study showed
increased phagocytosis by neutrophils in RA patients who were positive for
anti-CCP and RF autoantibodies. Furthermore, there was an overall hyperactivation
of the phagocytes in RA patients. Our data suggest that anti-CCP and RF may
indirectly enhance the inflammation cascade involving neutrophils and may
indirectly sustain tissue damage in RA. Targeting the production of these
autoantibodies may be a promising strategy in the management of RA.