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Abstract Number: 2299

M-Ficolin and Masp-2 As Inflammatory Markers in Oligoarticular and Systemic Juvenile Idiopathic Arthritis

Christine Petri1, Steffen Thiel2, Jens Christian Jensenius2 and Troels Herlin1, 1Pediatric Rheumatology Clinic, Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark, 2Biomedicine, Aarhus University, Aarhus, Denmark

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: complement, innate immunity and juvenile idiopathic arthritis (JIA)

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Session Information

Title: Pediatric Rheumatology - Clinical and Therapeutic Aspects: Systemic Juvenile Idiopathic Arthritis, Spondyloarthropathy and Miscellaneous Pediatric Rheumatic Diseases

Session Type: Abstract Submissions (ACR)

Background/Purpose

The lectin pathway of the complement plays a crucial role in the pathogenesis of various inflammatory processes. The lectin pathway proteins are activated through the recognition of pathogens by the pattern recognition molecules (PRMs), which include the mannan-binding lectin (MBL), and H- and M-ficolin in collaboration with MBL-associated serine proteases (MASPs). PRMs reportedly play a role in rheumatoid arthritis (RA) indicating a correlation between the concentration of these proteins and RA disease activity. The aim was to evaluate the possible pathogenic role of the PRMs in Juvenile Idiopathic Arthritis (JIA).

Methods

We measured MBL, M-ficolin, H-ficolin, MASP-1, -2, -3, and the two alternative splice products, MAp44 and MAp19, in plasma and synovial fluid (SF) of 109 children with persistent oligoarticular JIA and 19 children with systemic JIA. The concentrations of the eight proteins were measured by in-house time-resolved immunoflurometric assays (TRIFMA) using monoclonal antibodies.

Results

We observed significantly higher levels of M-ficolin and MBL-associated serine proteases in plasma from patients with systemic JIA compared to persistent oligoarticular JIA (p<0.001). Notably higher levels of M-ficolin and MASP-2 were also found in synovial fluid from patients with systemic JIA (n=11) compared to SF from patients with oligoarticular JIA (n=36). Plasma/SF ratio of the lectin pathway proteins were calculated in paired samples for oligoarticular JIA (n=36) and systemic onset JIA (n=11). We observed significantly high plasma/SF for both subtypes for M- and H-ficolin, MASP-1 and -2, MAp44 and MAp19, but the MASP-3 levels was significantly higher in SF than in plasma for both subtypes. M-ficolin and MASP-2 was significantly related to erythrocyte sedimentation rate (ESR), C-reactive protein, white blood cell count, platelet count (p<0.001). In addition M-ficolin was significantly related to the number of active joints (p=0.008) and conversely related to hemoglobin levels (p=0.017).

Conclusion

Our results suggest plasma M-ficolin and MASP-2 as inflammatory markers in juvenile idiopathic arthritis. The level of the proteins is higher in plasma than in SF, except for MASP-3, indicating that MASP-3 may be secreted into or produced locally in the joint.


Disclosure:

C. Petri,
None;

S. Thiel,
None;

J. C. Jensenius,
None;

T. Herlin,
None.

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