title: An evaluation of anti-TNF-alpha-therapy in patients with ankylosing spondylitis: imbalanced activation of NF kappa B subunits in lymphocytes and modulation of serum cortisol concentration.
abstract: The aim of this study was to analyse patients with ankylosing spondylitis (AS) during the course of infliximab therapy. The molecular effects were evaluated using lymphocytes and sera that were isolated before therapy began, then again after 2 and 12 weeks from 17 AS patients and compared to those of 24 healthy control individuals. All 17 AS patients responded to treatment with infliximab as assessed using BASDAI. Elevated serum levels of IL-6, CRP and cortisol were reduced to normal levels by the 12 weeks time point. The level of DNA-binding p65 was decreased during the course of infliximab therapy whereas the level of DNA-binding p50 remained elevated until the 12 weeks time point. Taken together, Infliximab is an effective treatment for AS and results in decreased levels of the inflammation markers IL-6 and CRP, and of endogenous cortisol concentration. Unequal alterations in the levels of activated NF-kappaB subunits p50 and p65 might provide insights into the mechanisms of NF-kappaB action and anti-TNF-alpha therapy in AS.
authors.affiliation: Department of Internal Medicine and Center of Rheumatology, Rostock Clinic South, Südring 81, 18059 Rostock, Germany.
authors.forename: Martin
authors.initials: M
authors.lastname: Eggert
authors.forename: Ulrike
authors.initials: U
authors.lastname: Seeck
authors.forename: Marco
authors.initials: M
authors.lastname: Semmler
authors.forename: Ulrich
authors.initials: U
authors.lastname: Maass
authors.forename: Sabine
authors.initials: S
authors.lastname: Dietmann
authors.forename: Martin
authors.initials: M
authors.lastname: Schulz
authors.forename: Helmut
authors.initials: H
authors.lastname: Dotzlaw
authors.forename: Gunther
authors.initials: G
authors.lastname: Neeck
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000008:administration & dosage; D018501:Antirheumatic Agents / Q000008:administration & dosage; D015415:Biomarkers / Q000032:analysis / Q000097:blood; D002097:C-Reactive Protein / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood* / Q000276:immunology; D000069285:Infliximab; D015850:Interleukin-6 / Q000097:blood; D008214:Lymphocytes / Q000187:drug effects* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D016328:NF-kappa B / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D052002:NF-kappa B p50 Subunit / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000188:drug therapy* / Q000276:immunology*; D051996:Transcription Factor RelA / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D015533:Transcriptional Activation / Q000187:drug effects / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D015415:Biomarkers; D004268:DNA-Binding Proteins; D015850:Interleukin-6; D016328:NF-kappa B; D052002:NF-kappa B p50 Subunit; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069285:Infliximab; D006854:Hydrocortisone