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24. Plasma microfibrillar-associated protein 4 is not prognostic of emphysema progression but is associated with cardiovascular disease history and mortality in COPD patients

Author

Johansson, Sofie Lock, primary, Wulf-Johansson, Helle, additional, Schlosser, Anders, additional, Titlestad, Ingrid L., additional, Miller, Bruce, additional, Tal-Singer, Ruth, additional, Holmskov, Uffe, additional, Vestbo, Jørgen, additional, and Sørensen, Grith Lykke, additional

Published
2019
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25. Direct-acting antivirals-based therapy decreases hepatic fibrosis serum biomarker microfibrillar-associated protein 4 in hepatitis C patients

Author

Mölleken, Christian, Ahrens, Maike, Schlosser, Anders, Dietz, Julia, Eisenacher, Martin, Meyer, Helmut E., Schmiegel, Wolff, Holmskov, Uffe, Sarrazin, Christoph, Sørensen, Grith Lykke, Sitek, Barbara, Bracht, Thilo, Mölleken, Christian, Ahrens, Maike, Schlosser, Anders, Dietz, Julia, Eisenacher, Martin, Meyer, Helmut E., Schmiegel, Wolff, Holmskov, Uffe, Sarrazin, Christoph, Sørensen, Grith Lykke, Sitek, Barbara, and Bracht, Thilo

Abstract

Background/Aims: An estimated 80 million people worldwide are infected with viremic hepatitis C virus (HCV). Even after eradication of HCV with direct acting antivirals (DAAs), hepatic fibrosis remains a risk factor for hepatocarcinogenesis. Recently, we confirmed the applicability of microfibrillar-associated protein 4 (MFAP4) as a serum biomarker for the assessment of hepatic fibrosis. The aim of the present study was to assess the usefulness of MFAP4 as a biomarker of liver fibrosis after HCV eliminating therapy with DAAs. Methods: MFAP4 was measured using an immunoassay in 50 hepatitis C patients at baseline (BL), the end-of-therapy (EoT), and the 12-week follow-up visit (FU). Changes in MFAP4 from BL to FU and their association with laboratory parameters including alanine aminotransferase (ALT), aspartate aminotransferase (AST), platelets, the AST to platelet ratio index (APRI), fibrosis-4 score (FIB-4), and albumin were analyzed. Results: MFAP4 serum levels were representative of the severity of hepatic fibrosis at BL and correlated well with laboratory parameters, especially APRI (Spearman correlation, R²=0.80). Laboratory parameters decreased significantly from BL to EoT. MFAP4 serum levels were found to decrease from BL and EoT to FU with high statistical significance (Wilcoxon p<0.001 for both). Conclusions: Our findings indicate that viral eradication resulted in reduced MFAP4 serum levels, presumably representing a decrease in hepatic fibrogenesis or fibrosis. Hence, MFAP4 may be a useful tool for risk assessment in hepatitis C patients with advanced fibrosis after eradication of the virus.

Published
2018

26. Impact of red and processed meat and fibre intake on treatment outcomes among patients with chronic inflammatory diseases:protocol for a prospective cohort study of prognostic factors and personalised medicine

Author

Christensen, Robin, Heitmann, Berit L., Andersen, Karina Winther, Nielsen, Ole Haagen, Sørensen, Signe Bek, Jawhara, Mohamad, Bygum, Anette, Hvid, Lone, Grauslund, Jakob, Wied, Jimmi, Glerup, Henning, Fredberg, Ulrich, Villadsen, Jan Alexander, Kjær, Søren Geill, Fallingborg, Jan, Moghadd, Seyed A. G. R., Knudsen, Torben, Brodersen, Jacob, Frøjk, Jesper, Dahlerup, Jens Frederik, Bojesen, Anders Bo, Sørensen, Grith Lykke, Thiel, Steffen, Færgeman, Nils J., Brandslund, Ivan, Bennike, Tue Bjerg, Stensballe, Allan, Schmidt, Erik Berg, Franke, Andre, Ellinghaus, David, Rosenstiel, Philip, Raes, Jeroen, Boye, Mette, Werner, Lars, Nielsen, Charlotte Lindgaard, Munk, Heidi Lausten, Nexoe, Anders Bathum, Ellingsen, Torkell, Holmskov, Uffe, Kjeldsen, Jens, Andersen, Vibeke, Christensen, Robin, Heitmann, Berit L., Andersen, Karina Winther, Nielsen, Ole Haagen, Sørensen, Signe Bek, Jawhara, Mohamad, Bygum, Anette, Hvid, Lone, Grauslund, Jakob, Wied, Jimmi, Glerup, Henning, Fredberg, Ulrich, Villadsen, Jan Alexander, Kjær, Søren Geill, Fallingborg, Jan, Moghadd, Seyed A. G. R., Knudsen, Torben, Brodersen, Jacob, Frøjk, Jesper, Dahlerup, Jens Frederik, Bojesen, Anders Bo, Sørensen, Grith Lykke, Thiel, Steffen, Færgeman, Nils J., Brandslund, Ivan, Bennike, Tue Bjerg, Stensballe, Allan, Schmidt, Erik Berg, Franke, Andre, Ellinghaus, David, Rosenstiel, Philip, Raes, Jeroen, Boye, Mette, Werner, Lars, Nielsen, Charlotte Lindgaard, Munk, Heidi Lausten, Nexoe, Anders Bathum, Ellingsen, Torkell, Holmskov, Uffe, Kjeldsen, Jens, and Andersen, Vibeke

Published
2018

30. Alterations of the murine gut microbiome in allergic airway disease are independent of surfactant protein D

Author

Barfod, Kenneth Klingenberg, Roggenbuck, Michael, Al-Shuweli, Suzan, Fakih, Dalia, Sørensen, Søren Johannes, Sørensen, Grith Lykke, Barfod, Kenneth Klingenberg, Roggenbuck, Michael, Al-Shuweli, Suzan, Fakih, Dalia, Sørensen, Søren Johannes, and Sørensen, Grith Lykke

Abstract

Background SP-D is an important host defense lectin in innate immunity and SP-D deficient mice show several abnormal immune effects and are susceptible to allergen-induced airway disease. At the same time, host microbiome interactions play an important role in the development of allergic airway disease, and alterations to gut microbiota have been linked to airway disease through the gut-lung axis. Currently, it is unknown if the genotype (Sftpd-/- or Sftpd+/+) of the standard SP-D mouse model can affect the host microbiota to such an degree that it would overcome the cohousing effect on microbiota and interfere with the interpretation of immunological data from the model. Generally, little is known about the effect of the SP-D protein in itself and in combination with airway disease on the microbiota. In this study, we tested the hypothesis that microbiome composition would change with the lack of SP-D protein and presence of allergic airway disease in the widely used SP-D-deficient mouse model. Results We describe here for the first time the lung and gut microbiota of the SP-D mouse model with OVA induced allergic airway disease. After the challenge animals were killed and fecal samples were taken from the caecum and lungs were subjected to bronchoalveolar lavage for comparison of gut and lung microbiota by Illumina 16S rRNA gene sequencing. A significant community shift was observed in gut microbiota after challenge with OVA. However, the microbial communities were not significantly different between SP-D deficient and wild type mice from the same cages in either naïve or OVA treated animals. Wild type animals did however show the largest variation between mice. Conclusions Our results show that the composition of the microbiota is not influenced by the SP-D deficient genotype under naïve or OVA induced airway disease. However, OVA sensitization and pulmonary challenge did alter the gut microbiota, supporting a bidirectional lung-gut crosstalk. Future mechanist

Published
2017

31. Localization and distribution offibrinogen C domain containing 1(FIBCD1) in human tissues

Author

von Huth, Sebastian, Møller, Jesper Bonnet, Schlosser, Anders, Marcussen, Niels, Nielsen, Ole, Pilecki, Bartosz, Jepsen, Christine Elise Schøler, Sørensen, Grith Lykke, and Holmskov, Uffe

Abstract

Introduction: We have previously identified and characterized fibrinogen C domain-containing 1 (FIBCD1) as a homotetrameric type II transmembrane protein. FIBCD1 is a member of the fibrinogen- related protein (FReP) family, and is thought to play a crucial role in the innate immune system (Schlosser et al, 2009; Thomsen et al, 2011).FIBCD1 functions as an endocytic receptor, binding chitin and other acetylated compounds with high affinity. We hypothesize that FIBCD1 serves as a pattern recognition molecule for acetylated compounds, found in various pathogens such as helminths and fungi. We have previously shown that FIBCD1 is present at mucosal surfaces in the lung and large intestine.Aim: The present study investigates the distribution and localization of FIBCD1 in various healthy human tissues.Results: We used a monoclonal antibody directed towards the FIBCD1 ectodomain in an immunohistochemistry-based analysis and demonstrate that FIBCD1 protein is highly expressed at the apical surfaces of the epithelium throughout the gastrointestinal tract, in the uterus, testis, bladder, gallbladder and the salivary glands. To a lesser extent, FIBCD1 is expressed in the pancreas, the spleen and the tonsils.Moreover, using quantitative real-time PCR we demonstrate that FIBCD1 mRNA is highly expressed in the gastrointestinal tract, the lung, the adrenal gland and the testis, which is in coherence with our immunohistochemical findings.Conclusion: FIBCD1 is present at the apical epithelial surfaces of various mucosal tissues. This strengthens our hypothesis that FIBCD1 is a novel player involved in the innate immune responses of the mucosa.

Published
2016

35. Increasing antiviral activity of surfactant protein d trimers by introducing residues from bovine serum collectins: dissociation of mannan-binding and antiviral activity

Author

Hartshorn, K L, White, M R, Smith, K, Sorensen, G, Kuroki, Y, Holmskov, U, Head, J, Crouch, E C, and Sørensen, Grith Lykke

Subjects
Glycan, Glycoconjugate, Immunology, Amino Acid Motifs, Collectin, Enzyme-Linked Immunosorbent Assay, Article, Cell Line, Mannans, Conglutinin, Influenza, Human, Humans, Bovine serum albumin, Pulmonary Surfactant-Associated Protein D, Mannan, chemistry.chemical_classification, biology, Mannan binding, General Medicine, Hemagglutination Inhibition Tests, Collectins, Recombinant Proteins, Biochemistry, chemistry, Influenza A virus, biology.protein
Abstract

Collectins contribute to host defence through interactions with glycoconjugates on pathogen surfaces. We have prepared recombinant trimeric neck and carbohydrate recognition domains (NCRD) of collectins, and we now show that the NCRD of bovine conglutinin and CL-46 (like that of CL-43) have greater intrinsic antiviral activity for influenza A virus (IAV) than the human SP-D NCRD (hSP-D-NCRD). The three serum collectins differ from SP-D by having insertions adjacent to amino acid 325 and substitution of hydrophobic residues for arginine 343. We previously showed that a three amino acid (RAK) insertion, as found in CL-43, increases antiviral activity and mannan-binding activity of the hSP-D-NCRD, while the substitution of valine at 343, as in conglutinin, more strongly increased these activities. Mannan-binding activity of collectins has been considered to predict for ability to bind to high mannose glycans on viruses or other pathogens. We now show, however, that combined mutants containing the RAK insertion and R343V or R343I substitutions have greatly increased mannan-binding ability, but lower IAV binding or inhibiting activity than mutants containing R343V or R343I substitutions only. These findings indicate differences in the recognition of glycan structures of mannan and IAV by the NCRD and emphasize the importance of the flanking sequences in determining the differing interactions of human SP-D and bovine serum collectins with mannose-rich glycoconjugates on IAV and other pathogens. Of interest, we show conservation of some monoclonal antibody-binding epitopes between bovine collectin NCRD and hSP-D, suggesting shared structural motifs.

Published
2010

36. No effect of ablation of surfactant protein-D on acute cerebral infarction in mice

Author

Lambertsen, Kate Lykke, Østergaard, Kamilla, Clausen, Bettina Hjelm, Hansen, Søren, Stenvang, Jan, Thorsen, Stine Buch, Meldgaard, Michael, Kristensen, Bjarne Winther, Hansen, Pernille B. Lærkegaard, Sørensen, Grith Lykke, Finsen, Bente, Lambertsen, Kate Lykke, Østergaard, Kamilla, Clausen, Bettina Hjelm, Hansen, Søren, Stenvang, Jan, Thorsen, Stine Buch, Meldgaard, Michael, Kristensen, Bjarne Winther, Hansen, Pernille B. Lærkegaard, Sørensen, Grith Lykke, and Finsen, Bente

Abstract

BACKGROUND: Crosstalk between the immune system in the brain and the periphery may contribute to the long-term outcome both in experimental and clinical stroke. Although, the immune defense collectin surfactant protein-D (SP-D) is best known for its role in pulmonary innate immunity, SP-D is also known to be involved in extrapulmonary modulation of inflammation in mice. We investigated whether SP-D affected cerebral ischemic infarction and ischemia-induced inflammatory responses in mice.METHODS: The effect of SP-D was studied by comparing the size of ischemic infarction and the inflammatory and astroglial responses in SP-D knock out (KO) and wild type (WT) mice subjected to permanent middle cerebral artery occlusion. SP-D mRNA production was assessed in isolated cerebral arteries and in the whole brain by PCR, and SP-D protein in normal appearing and ischemic human brain by immunohistochemistry. Changes in plasma SP-D and TNF were assessed by ELISA and proximity ligation assay, respectively.RESULTS: Infarct volumetric analysis showed that ablation of SP-D had no effect on ischemic infarction one and five days after induction of ischemia. Further, ablation of SP-D had no effect on the ischemia-induced increase in TNF mRNA production one day after induction of ischemia; however the TNF response to the ischemic insult was affected at five days. SP-D mRNA was not detected in parenchymal brain cells in either naïve mice or in mice subjected to focal cerebral ischemia. However, SP-D mRNA was detected in middle cerebral artery cells in WT mice and SP-D protein in vascular cells both in normal appearing and ischemic human brain tissue. Measurements of the levels of SP-D and TNF in plasma in mice suggested that levels were unaffected by the ischemic insult. Microglial-leukocyte and astroglial responses were comparable in SP-D KO and WT mice.CONCLUSIONS: SP-D synthesis in middle cerebral artery cells is consistent with SP-D conceivably leaking into the

Published
2014

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

Author

Høgh, Silje Vermedal, Lindegaard, Hanne Merete, Sørensen, Grith Lykke, Høj, A, Bendixen, C, Junker, Peter, and Holmskov, Uffe

Subjects
Adult, Male, Threonine, Adolescent, Genotype, Variation (Genetics), Middle Aged, Pulmonary Surfactant-Associated Protein D, Arthritis, Rheumatoid, Methionine, Humans, Female, Prospective Studies, Aged
Abstract

Udgivelsesdato: Jan Innate immune system abnormalities, e.g., mannan-binding lectin (MBL) genotype variants, have been demonstrated to modify the disease course of rheumatoid arthritis (RA). Surfactant protein D (SP-D) shares important structural and functional properties with MBL suggesting that SP-D may be an additional RA disease modifier. The Met11Thr polymorphism in the N-terminal part of SP-D is an important determinant for the SP-D serum level, but this polymorphism is also essential to the function and assembly into oligomers. We aimed to compare the serum levels of SP-D in a cohort of newly diagnosed untreated RA patients with healthy matched controls, and to investigate if there was an association to core measures of disease activity within the first year after disease onset. Secondly, we aimed to investigate whether the Met11Thr polymorphism was associated with RA. Serum SP-D was significantly lower in DMARD naive RA patients compared with healthy controls (P = 0.016). Median SP-D concentration at inclusion was 878 ng/ml (95% CI: 730-1033) and 1164 ng/ml (95% CI: 1093-1366) in RA patients and matched controls, respectively. SP-D increased during Methotrexate treatment (P < 0.0001), and at 1-year follow-up median SP-D was 1032 ng/ml (95% CI: 777-1255). SP-D levels did not correlate with traditional disease activity measures. The Thr11/Thr11 genotype and the Thr11 allele tended to be more frequent in RA patients. In conclusion, the low serum level of SP-D and the lack of correlation with traditional disease activity measures indicate that SP-D reflects a distinctive aspect in the RA pathogenesis.

Published
2008

38. Plasma surfactant protein D levels and the relation to body mass index in a chinese population

Author

Zhao, X M, Wu, Y P, Wei, R, Cai, H X, Tornoe, I, Han, J J, Wang, Y, de Groot, P G, Holmskov, U, Xia, Z L, and Sørensen, Grith Lykke

Subjects
Adult, Asian Continental Ancestry Group, Male, Sex Factors, Age Factors, Humans, Female, Obesity, Middle Aged, Pulmonary Surfactant-Associated Protein D, Body Mass Index
Abstract

Udgivelsesdato: 2007-Jul Surfactant protein D (SP-D) is a member of the collectin family and is an important component of the pulmonary innate host defence. The protein has a widespread distribution in the human body and is present in multiple epithelia, in endothelium and in blood. Various studies have looked at the relationship between serum SP-D levels and pulmonary inflammatory diseases. The SP-D distribution has been most thoroughly described in European populations and appears with a broad range of serum values highly influenced by genetic factors. In the present study, we investigated the plasma SP-D distribution in a Chinese population from the Tai An region comprising 268 individuals. We found that (i) plasma SP-D in the Chinese population was distributed with a median value of 380.2 ng/ml (324.9; 418.7) and a range from 79.4 to 3965.3 ng/ml, (ii) significantly higher plasma SP-D in men than in women, and no significant effect of age, and (iii) a significant inverse association between serum SP-D and body mass index (BMI) (P = 0.012). The data indicate that racial differences in SP-D expression exist as the median plasma SP-D in the Chinese population was approximately two times lower than the median serum SP-D previously measured in a Danish population using the same immuno-assay. The inverse association between serum SP-D and BMI found in the Chinese population indicates that serum SP-D is related to obesity in similar ways in Chinese and Danes.

Published
2007

39. Enzyme-Linked Immunosorbent Assay Characterization of Basal Variation and Heritability of Systemic Microfibrillar-Associated Protein 4

Author

Sækmose, Susanne Gjørup, primary, Schlosser, Anders, additional, Holst, René, additional, Johansson, Sofie Lock, additional, Wulf-Johansson, Helle, additional, Tornøe, Ida, additional, Vestbo, Jørgen, additional, Kyvik, Kirsten Ohm, additional, Barington, Torben, additional, Holmskov, Uffe, additional, and Sørensen, Grith Lykke, additional

Published
2013
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41. Circulating surfactant protein -D is low and correlates negatively with systemic inflammation in early, untreated rheumatoid arthritis

Author

Christensen, Anne Friesgaard, Sørensen, Grith Lykke, Hørslev-Petersen, Kim, Holmskov, Uffe, Lindegaard, Hanne Merete, Junker, Kirsten, Hetland, Merete Lund, Stengaard-Pedersen, Kristian, Jacobsen, Søren, Lottenburger, Tine, Ellingsen, Torkell, Andersen, Lis Smedegaard, Hansen, Ib, Skjødt, Henrik, Pedersen, Jens Kristian, Lauridsen, Ulrik Birk, Svendsen, Anders, Tarp, Ulrik, Pødenphant, Jan, Vestergaard, Aage, Jurik, Anne Grethe, Østergaard, Mikkel, Junker, Peter, Christensen, Anne Friesgaard, Sørensen, Grith Lykke, Hørslev-Petersen, Kim, Holmskov, Uffe, Lindegaard, Hanne Merete, Junker, Kirsten, Hetland, Merete Lund, Stengaard-Pedersen, Kristian, Jacobsen, Søren, Lottenburger, Tine, Ellingsen, Torkell, Andersen, Lis Smedegaard, Hansen, Ib, Skjødt, Henrik, Pedersen, Jens Kristian, Lauridsen, Ulrik Birk, Svendsen, Anders, Tarp, Ulrik, Pødenphant, Jan, Vestergaard, Aage, Jurik, Anne Grethe, Østergaard, Mikkel, and Junker, Peter

Abstract

Surfactant protein D (SP-D) is a collectin with immuno-regulatory functions, which may depend on oligomerization. Anti-microbial and anti-inflammatory properties have been attributed to multimeric SP-D variants, while trimeric subunits per se have been suggested to enhance inflammation. Previously, we reported low circulating SP-D in early rheumatoid arthritis (RA), and the present investigation aims to extend these data by serial SP-D serum measurements, studies on synovial fluid, SP-D size distribution and genotyping in patients with early RA.

Published
2010

44. Type I and III collagen turnover is increased in axial spondyloarthritis and psoriatic arthritis. Associations with disease activity and diagnostic capacity.

Author

Gudmann NS, Siebuhr AS, Christensen AF, Ejstrup L, Sørensen GL, Loft AG, Karsdal MA, Bay-Jensen AC, Munk HL, and Junker P

Subjects
Adult, Area Under Curve, Arthritis, Psoriatic genetics, Case-Control Studies, Enzyme-Linked Immunosorbent Assay, Female, HLA-B27 Antigen genetics, Humans, Male, ROC Curve, Radioimmunoassay, Severity of Illness Index, Spondylarthropathies genetics, Spondylarthropathies metabolism, Arthritis, Psoriatic metabolism, Collagen Type I metabolism, Collagen Type III metabolism, Peptides metabolism
Abstract

Objectives: To investigate the turnover of type I and III collagen by neo-epitope markers in patients with axial spondyloarthritis (axSpA) and psoriatic arthritis (PsA)., Methods: Patients with PsA (n=101) or axSpA (n=110) and healthy subjects (n=120) were included. Demographic and clinical data were recorded. Markers of type I and III collagen were quantified by RIA (ICTP) or ELISA (C1M and C3M). Non-parametric statistics were applied for intergroup comparisons and correlation studies. The diagnostic potential of these marker molecules was assessed by ROC analysis., Results: C1M and C3M, which originate from soft connective tissues, were significantly higher in axSpA and PsA as compared with healthy control subjects. CIM and C3M correlated with ASDAS and DAS28. Overall, ICTP, which arises from bone degradation, did not differ between disease versus healthy. However, ICTP was lower in HLA-B27 positive than in HLA-B27 negative patients with axSpA. There was no association between bone and soft connective tissue collagen I markers (ICTP and C1M), while C1M and C3M were highly correlated (p<0.0001). C1M discriminated between healthy and diseased with AUCs of 0.83 for PsA and 0.79 for axSpA. C3M AUCs were 0.77 for PsA and 0.78 for axSpA., Conclusions: Type I and III collagen remodelling in soft connective tissue is increased in axSpA and PsA and associates with disease activity. Bone collagen degradation is lower in HLA-B27 positive compared with HLA-B27 negative axSpA, which may represent an aspect of enhanced enthesopathic bone proliferation in HLA-B27 carriers. C1M and C3M distinguish well between healthy and diseased individuals.

Published
2017

45. Circulating surfactant protein -D is low and correlates negatively with systemic inflammation in early, untreated rheumatoid arthritis.

Author

Christensen AF, Sørensen GL, Hørslev-Petersen K, Holmskov U, Lindegaard HM, Junker K, Hetland ML, Stengaard-Pedersen K, Jacobsen S, Lottenburger T, Ellingsen T, Andersen LS, Hansen I, Skjødt H, Pedersen JK, Lauridsen UB, Svendsen A, Tarp U, Pødenphant J, Vestergaard A, Jurik AG, Østergaard M, and Junker P

Subjects
Adolescent, Adult, Aged, Arthritis, Rheumatoid genetics, Arthritis, Rheumatoid physiopathology, Arthrography, Female, Genotype, Health Status, Humans, Male, Metallothionein genetics, Middle Aged, Polymorphism, Single Nucleotide, Prospective Studies, Reference Values, Surveys and Questionnaires, Young Adult, Arthritis, Rheumatoid blood, Pulmonary Surfactant-Associated Protein D blood
Abstract

Introduction: Surfactant protein D (SP-D) is a collectin with immuno-regulatory functions, which may depend on oligomerization. Anti-microbial and anti-inflammatory properties have been attributed to multimeric SP-D variants, while trimeric subunits per se have been suggested to enhance inflammation. Previously, we reported low circulating SP-D in early rheumatoid arthritis (RA), and the present investigation aims to extend these data by serial SP-D serum measurements, studies on synovial fluid, SP-D size distribution and genotyping in patients with early RA., Methods: One-hundred-and-sixty disease-modifying antirheumatic drug (DMARD) naïve RA patients with disease duration less than six months were studied prospectively for four years (CIMESTRA (Ciclosporine, Methotrexate, Steroid in RA) trial) including disease activity measures (C-reactive protein, joint counts and Health Assessment Questionnaire (HAQ) score), autoantibodies, x-ray findings and SP-D. SP-D was quantified by enzyme-linked immunosorbent assay (ELISA) and molecular size distribution was assessed by gel filtration chromatography. Further, SP-D Met11Thr single nucleotide polymorphism (SNP) analysis was performed., Results: Serum SP-D was significantly lower in RA patients at baseline compared with healthy controls (P < 0.001). SP-D increased slightly during follow-up (P < 0.001), but was still subnormal at four years after adjustment for confounders (P < 0.001). SP-D in synovial fluid was up to 2.5-fold lower than in serum. While multimeric variants were detected in serum, SP-D in synovial fluid comprised trimeric subunits only. There were no significant associations between genotype distribution and SP-D. Baseline SP-D was inversely associated to CRP and HAQ score. A similar relationship was observed regarding temporal changes in SP-D and CRP (zero to four years). SP-D was not associated to x-ray findings., Conclusions: This study confirms that circulating SP-D is persistently subnormal in early and untreated RA despite a favourable therapeutic response obtained during four years of follow-up. SP-D correlated negatively to disease activity measures, but was not correlated with x-ray progression or SP-D genotype. These observations suggest that SP-D is implicated in RA pathogenesis at the protein level. The exclusive presence of trimeric SP-D in affected joints may contribute to the maintenance of joint inflammation., Trial Registration: (j.nr NCT00209859).

Published
2010
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