Circulating surfactant protein D is decreased in early rheumatoid arthritis: a 1-year prospective study

S V Hoegh1, H M Lindegaard, G L Sorensen

  • 1Medical Biotechnology Center, Institute of Medical Biology, University of Southern Denmark, Odense, Denmark.

Insights

Lower surfactant protein D (SP-D) levels in rheumatoid arthritis (RA) patients may indicate a distinct role in disease pathogenesis. SP-D levels were lower in new RA patients and did not correlate with disease activity, but a specific SP-D genotype was more frequent in RA.

Area of Science:

  • Immunology
  • Rheumatology
  • Genetics

Background:

  • Innate immune system abnormalities, such as mannan-binding lectin (MBL) genotype variants, influence rheumatoid arthritis (RA) disease progression.
  • Surfactant protein D (SP-D) shares structural and functional similarities with MBL, suggesting its potential role as an RA disease modifier.
  • The Met11Thr polymorphism in SP-D affects serum levels, oligomerization, and function.

Purpose of the Study:

  • To compare serum SP-D levels in newly diagnosed, untreated RA patients versus healthy controls.
  • To investigate the association between SP-D levels and RA disease activity measures within the first year of onset.
  • To examine the association of the Met11Thr SP-D polymorphism with RA.

Main Methods:

  • Serum SP-D levels were measured in 140 DMARD-naive RA patients and 140 matched healthy controls.
  • SP-D levels were assessed at diagnosis and at 1-year follow-up, with correlation to disease activity scores.
  • Genotyping for the Met11Thr SP-D polymorphism was performed.

Main Results:

  • Serum SP-D levels were significantly lower in DMARD-naive RA patients (median 878 ng/ml) compared to healthy controls (median 1164 ng/ml).
  • SP-D levels increased during methotrexate treatment, reaching a median of 1032 ng/ml at 1-year follow-up.
  • SP-D levels did not correlate with traditional RA disease activity measures. The Thr11/Thr11 genotype and Thr11 allele were more frequent in RA patients.

Conclusions:

  • Low serum SP-D levels in early RA suggest a distinct pathogenic role, independent of traditional disease activity markers.
  • The Met11Thr polymorphism may be associated with RA susceptibility.
  • SP-D's role in RA pathogenesis warrants further investigation.