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SAT0028 Circulating Surfactant Protein-D (SP-D) Molecular Size Profile Differs between Patients with Untreated Axial Spondyloarthritis and Healthy Control Subjects
  1. H.L. Munk1,2,
  2. D. Fakih3,4,
  3. G.L. Sorensen4,
  4. Q. Tan5,
  5. L. Christiansen5,
  6. A.F. Christensen6,
  7. L. Ejstrup7,
  8. A.G. Loft6,8,
  9. K.O. Kyvik2,
  10. R. Jounblat3,9,
  11. U. Holmskov4,
  12. P. Junker1,2
  1. 1Department of Rheumatology, Odense University Hospital
  2. 2Department of Clinical Research, University of Southern Denmark, Odense, Denmark
  3. 3Laboratory of Immunology, Faculty of Public Health, Lebanese University, Fanar, Lebanon
  4. 4Department of Cancer and Inflammation Research, Institute of Molecular Medicine
  5. 5Department of Epidemiology, Biostatistics and Biodemography, University of Southern Denmark, Odense
  6. 6Department of Internal Medicine, Vejle Hospital, Vejle
  7. 7Department of Rheumatology, Esbjerg Hospital, Esbjerg
  8. 8Department of Rheumatology, Aahus University Hospital, Aahus, Denmark
  9. 9Department of Biology, Faculty og Sciences II, Lebanese University, Fanar, Lebanon


Background Surfactant protein-D (SP-D), an innate immune defence molecule of the collectin family has immune modulatory and anti-microbial effects and is expressed in lungs and on mucosal surfaces. The molecule consists of subunits ordered as trimers, dodecamers and even higher multimers. In healthy adults genes are responsible for the majority of the quantitative variation of SP-D in serum as well as its molecular size distribution1. High Molecular weight (HMw) SP-D is suggested to have anti-inflammatory properties, while low Mw (LMw) variants lack this capacity. In spondyloarthritis (SpA) SP-D correlates negatively with hsCRP and positively with patient global assessment. LMw variants have been shown to prevail in serum during inflammatory flares in chronic obstructive pulmonary disease.

Objectives To investigate the distribution of SP-D HMw and LMw variants in serum among patients with SpA and controls according to the Met11Thr polymorphism.

Methods 34 patients with SpA (age 22–63) according to the ASAS criteria, receiving NSAIDs only and 57 healthy controls (age 10–75) were included (Table 1). Total SP-D in serum was measured by ELISA and SNP rs721917 was genotyped. SP-D molecular size distribution was assessed using gel filtration chromatography. Integration of the area under the curves was performed to determine the ratio between HMw and LMw SP-D in serum.

Results SP-D in SpA was in the normal range, 1092 ng/ml (725;1541) vs. controls, 910 ng/ml (494; 1682). Whereas the ratio of HMw:LMw serum SP-D was lower in SpA patients, 0.38 (0.18;0.53) compared to controls 1.49 (0.37; 3.24) even when adjusting for the Met11Thr polymorphism, gender, age, BMI and smoking (Table 2).

Tabel 1. Characteristics of patients and controls

Tabel 2. Ratio of HMw and LMw serum SP-D ratio between controls and SpA according to Met11Thr polymorphism

Conclusions The molecular size distribution of circulating SP-D in patients with SpA is skewed towards preponderance of small size molecular variants. SpA related disease mechanisms may disrupt the multimeric state of SP-D, thereby amplifying the inflammatory burden of the disease.

  1. Leth-Larsen R. J Immunol 2005;174:1532–8

Disclosure of Interest None declared

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