Proteomic analysis of synovial fluid from rheumatic arthritis and spondyloarthritis patients

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

DOI

  • Svend Birkelund, Aalborg Universitet
  • ,
  • Tue Bjerg Bennike, Aalborg Universitet
  • ,
  • Kenneth Kastaniegaard, Aalborg Universitet, Biogenity
  • ,
  • Mads Lausen, Aalborg Universitet
  • ,
  • Thomas Bouet Guldbæk Poulsen, Aalborg Universitet
  • ,
  • Tue Wenzel Kragstrup
  • Bent Winding Deleuran
  • Gunna Christiansen, Aalborg Universitet
  • ,
  • Allan Stensballe, Aalborg Universitet

Background: The aetiologies and pathogeneses of the joint diseases rheumatoid arthritis (RA) and spondyloarthritis (SpA) are still not fully elucidated. To increase our understanding of the molecular pathogenesis, we analysed the protein composition of synovial fluid (SF) from rheumatoid arthritis (RA) and spondyloarthritis (SpA) patients.

Methods: Fifty-six synovial fluid samples (RA, n = 32; SpA, n = 24) were digested with trypsin, and the resulting peptides were separated by liquid chromatography and analysed by tandem mass spectrometry. Additionally, the concentration of cell-free DNA (cfDNA) in the synovial fluid was measured, and plasma C-reactive protein (CRP) was determined.

Results: Three hundred thirty five proteins were identified within the SF. The more abundant proteins seen in RA SF were inflammatory proteins, including proteins originating from neutrophil granulocytes, while SpA SF had less inflammatory proteins and a higher concentration of haptoglobin. The concentration of cell-free DNA in the SF increased together with proteins that may have originated from neutrophils. Plasma CRP levels in both RA and SpA, correlated to other acute phase reactants.

Conclusions: The proteomic results underline that neutrophils are central in the RA pathology but not in SpA, and even though inhibitors of neutrophils (migration, proteinase inhibitors) were present in the SF it was not sufficient to interrupt the disease process.

OriginalsprogEngelsk
Artikelnummer29
TidsskriftClinical Proteomics
Vol/bind17
Antal sider15
ISSN1542-6416
DOI
StatusUdgivet - aug. 2020

Se relationer på Aarhus Universitet Citationsformater

ID: 194481085