Circulating surfactant protein D is decreased in systemic lupus erythematosus

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  • Silje Vermedal Hoegh, Danmark
  • Anne Voss, Danmark
  • Grith Lykke Sorensen, Danmark
  • Anette Høj, Danmark
  • Christian Bendixen
  • Peter Junker, Danmark
  • Uffe Holmskov, Danmark
  • Molekylær Genetik og Systembiologi
  • Institut for Genetik og Bioteknologi

Objective. Deficiencies of innate immune molecules like mannan binding lectin (MBL) have been implicated in the pathogenesis of systemic lupus erythematosus (SLE). Surfactant protein D (SP-D) and MBL belong to the same family of innate immune molecules - the collectins, which share important structural and functional properties. We aimed to compare concentrations of serum SP-D in patients with SLE and in healthy controls, and to investigate if SP-D is associated with selected disease indicators. We investigated the possible association of the Met11Thr polymorphism with disease, since this polymorphism is an important determinant for serum level, oligomerization pattern, and function of SP-D.

Methods. Serum SP-D was measured using a 5-layer ELISA in 70 SLE patients and 1476 healthy subjects. DNA was genotyped for the Met11Thr variant.

Results. Median SP-D level in serum was 911 ng/ml (95% CI 776-1118) in patients and 1068 ng/ml (95% CI 901-1246) in controls (p = 0.0004). Circulating SP-D did not differ significantly in patients with high, intermediate, or low SLE disease activity. Similarly, SP-D did not correlate with C-reactive protein, erythrocyte sedimentation rate, and anti-dsDNA seropositivity. Genetic analysis did not support an association of the Met11Thr genotype with SLE.

Conclusion. These findings suggest that low SP-D, unrelated to conventional disease indicators, represents an aspect of SLE etiopathogenesis.

TidsskriftJournal of Rheumatology
Sider (fra-til)2449-2453
Antal sider5
StatusUdgivet - 2009

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