From gene expression to serum proteins: biomarker discovery in ankylosing spondylitis

Objectives:Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS).Methods:Gene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results...

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Vydáno v:	Annals of the rheumatic diseases Ročník 69; číslo 1; s. 297 - 300
Hlavní autoři:	Haroon, N, Tsui, F W L, O’Shea, F D, Chiu, B, Tsui, H W, Zhang, H, Marshall, K W, Inman, R D
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	England BMJ Publishing Group Ltd and European League Against Rheumatism 01.01.2010 Elsevier Limited
Témata:	Adult Antibodies, Monoclonal - therapeutic use Antirheumatic Agents - therapeutic use Biomarkers - blood Blood Proteins - metabolism Blood Sedimentation C-Reactive Protein - metabolism Disease Female Gene expression Gene Expression Profiling - methods Humans Hypotheses Infliximab Laboratories Light Male Middle Aged Oligonucleotide Array Sequence Analysis - methods Patients Reverse Transcriptase Polymerase Chain Reaction - methods Severity of Illness Index Spondylitis, Ankylosing - blood Spondylitis, Ankylosing - drug therapy Tumor Necrosis Factor Ligand Superfamily Member 14 - blood Tumor necrosis factor-TNF Young Adult California
ISSN:	0003-4967, 1468-2060, 1468-2060
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Abstract	Objectives:Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS).Methods:Gene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results were confirmed by quantitative real-time (qRT)–PCR. Corresponding serum-soluble LIGHT (sLIGHT) was estimated by ELISA and the fold change in sLIGHT was correlated to the fold change in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and the Bath AS disease activity index.Results:Post-infliximab, 69% of the patients (11/16) achieved an ASAS20 response. Six candidate genes were differentially expressed by microarray; four of which were validated by qRT–PCR. sLIGHT showed the most significant difference. There was good correlation of baseline sLIGHT with CRP (R = 0.60; p = 0.01) and ESR (R = 0.51; p = 0.04). The fold change in sLIGHT correlated with change in both CRP (R = 0.71, p = 0.002) and ESR (R = 0.77, p<0.001).Conclusion:LIGHT is significantly downregulated by infliximab. sLIGHT correlated well with changes in inflammatory markers.
AbstractList	Objectives: Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS). Methods: Gene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results were confirmed by quantitative real-time (qRT)–PCR. Corresponding serum-soluble LIGHT (sLIGHT) was estimated by ELISA and the fold change in sLIGHT was correlated to the fold change in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and the Bath AS disease activity index. Results: Post-infliximab, 69% of the patients (11/16) achieved an ASAS20 response. Six candidate genes were differentially expressed by microarray; four of which were validated by qRT–PCR. sLIGHT showed the most significant difference. There was good correlation of baseline sLIGHT with CRP (R = 0.60; p = 0.01) and ESR (R = 0.51; p = 0.04). The fold change in sLIGHT correlated with change in both CRP (R = 0.71, p = 0.002) and ESR (R = 0.77, p<0.001). Conclusion: LIGHT is significantly downregulated by infliximab. sLIGHT correlated well with changes in inflammatory markers. Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS).OBJECTIVESStudying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS).Gene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results were confirmed by quantitative real-time (qRT)-PCR. Corresponding serum-soluble LIGHT (sLIGHT) was estimated by ELISA and the fold change in sLIGHT was correlated to the fold change in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and the Bath AS disease activity index.METHODSGene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results were confirmed by quantitative real-time (qRT)-PCR. Corresponding serum-soluble LIGHT (sLIGHT) was estimated by ELISA and the fold change in sLIGHT was correlated to the fold change in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and the Bath AS disease activity index.Post-infliximab, 69% of the patients (11/16) achieved an ASAS20 response. Six candidate genes were differentially expressed by microarray; four of which were validated by qRT-PCR. sLIGHT showed the most significant difference. There was good correlation of baseline sLIGHT with CRP (R = 0.60; p = 0.01) and ESR (R = 0.51; p = 0.04). The fold change in sLIGHT correlated with change in both CRP (R = 0.71, p = 0.002) and ESR (R = 0.77, p<0.001).RESULTSPost-infliximab, 69% of the patients (11/16) achieved an ASAS20 response. Six candidate genes were differentially expressed by microarray; four of which were validated by qRT-PCR. sLIGHT showed the most significant difference. There was good correlation of baseline sLIGHT with CRP (R = 0.60; p = 0.01) and ESR (R = 0.51; p = 0.04). The fold change in sLIGHT correlated with change in both CRP (R = 0.71, p = 0.002) and ESR (R = 0.77, p<0.001).LIGHT is significantly downregulated by infliximab. sLIGHT correlated well with changes in inflammatory markers.CONCLUSIONLIGHT is significantly downregulated by infliximab. sLIGHT correlated well with changes in inflammatory markers. Objectives: Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS). Methods: Gene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results were confirmed by quantitative real-time (qRT)â[euro]"PCR. Corresponding serum-soluble LIGHT (sLIGHT ) was estimated by ELISA and the fold change in sLIGHT was correlated to the fold change in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and the Bath AS disease activity index. Results: Post-infliximab, 69% of the patients (11/16) achieved an ASAS20 response. Six candidate genes were differentially expressed by microarray; four of which were validated by qRTâ[euro]"PCR. sLIGHT showed the most significant difference. There was good correlation of baseline sLIGHT with CRP (R â[euro]S=â[euro]S 0.60; pâ[euro]S=â[euro]S0.01) and ESR (R â[euro]S=â[euro]S 0.51; pâ[euro]S=â[euro]S0.04). The fold change in sLIGHT correlated with change in both CRP (R â[euro]S=â[euro]S 0.71, pâ[euro]S=â[euro]S0.002) and ESR (R â[euro]S=â[euro]S 0.77, p<0.001). Conclusion: LIGHT is significantly downregulated by infliximab. sLIGHT correlated well with changes in inflammatory markers. Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS). Gene expression changes were screened by microarray on peripheral blood RNA of 16 AS patients at baseline and 2 weeks post-infliximab, and selected results were confirmed by quantitative real-time (qRT)-PCR. Corresponding serum-soluble LIGHT (sLIGHT) was estimated by ELISA and the fold change in sLIGHT was correlated to the fold change in erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and the Bath AS disease activity index. Post-infliximab, 69% of the patients (11/16) achieved an ASAS20 response. Six candidate genes were differentially expressed by microarray; four of which were validated by qRT-PCR. sLIGHT showed the most significant difference. There was good correlation of baseline sLIGHT with CRP (R = 0.60; p = 0.01) and ESR (R = 0.51; p = 0.04). The fold change in sLIGHT correlated with change in both CRP (R = 0.71, p = 0.002) and ESR (R = 0.77, p<0.001). LIGHT is significantly downregulated by infliximab. sLIGHT correlated well with changes in inflammatory markers.
Author	Tsui, F W L Haroon, N Tsui, H W Marshall, K W Chiu, B Inman, R D Zhang, H O’Shea, F D
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/19103635$$D View this record in MEDLINE/PubMed
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Cites_doi	10.1002/art.23512 10.1093/rheumatology/41.7.759 10.1002/art.11104 10.1038/ng.2007.17 10.4049/jimmunol.174.2.646 10.1002/art.23523 10.1136/ard.2008.094870 10.1093/rheumatology/kem063 10.1038/sj.gene.6363975 10.1002/art.20852 10.1136/ard.2003.006916 10.1016/S1359-6101(03)00031-5 10.1146/annurev.immunol.23.021704.115719 10.1038/sj.gene.6363966 10.4049/jimmunol.169.12.6813
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Snippet	Objectives:Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS).Methods:Gene expression... Objectives: Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS). Methods: Gene... Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS). Gene expression changes were... Studying post-infliximab gene expression changes could provide insights into the pathogenesis of ankylosing spondylitis (AS).OBJECTIVESStudying post-infliximab...
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SubjectTerms	Adult Antibodies, Monoclonal - therapeutic use Antirheumatic Agents - therapeutic use Biomarkers - blood Blood Proteins - metabolism Blood Sedimentation C-Reactive Protein - metabolism Disease Female Gene expression Gene Expression Profiling - methods Humans Hypotheses Infliximab Laboratories Light Male Middle Aged Oligonucleotide Array Sequence Analysis - methods Patients Reverse Transcriptase Polymerase Chain Reaction - methods Severity of Illness Index Spondylitis, Ankylosing - blood Spondylitis, Ankylosing - drug therapy Tumor Necrosis Factor Ligand Superfamily Member 14 - blood Tumor necrosis factor-TNF Young Adult
Title	From gene expression to serum proteins: biomarker discovery in ankylosing spondylitis
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