title: Beneficial effects of cellular stress response in traditional spa treatment of rheumatoid arthritis.
abstract: Patients with rheumatoid arthritis often conduct bathing in hot mineral water with a high concentrations of sulfate compounds in the water and ambient air. We investigated the effect of hyperthermia and sulfur as possible stress factors at transcriptional level in several proinflammatory genes in fibroblast like synoviocytes. We mimicked the classical balneological treatment. Cells were exposed to 30 minutes of hyperthermia (41-42 degrees C) or sulfur (2 mM NaHS). Indeed, both factors were acting as stressors, inducing a profound expression of heat shock protein 70 (HSP70). Stimulation of the cells with IL1beta induced a series of proinflammatory genes (IL1alpha, IL1beta, TNFalpha, IL8, monocyte chemoattractant peptide-1 and COX-2), but if the cells were treated with hyperthermia prior to IL1beta expression, gene expressions were significantly decreased up to 8 h. Treatment with sulfur alone induced expression of observed genes up to 12 h. We may conclude that hyperthermia as a balneological mean has indeed a protective effect on cells, but sulfur, which at first we considered as an antiinflammatory mean, had actually an opposite effect and induced expression of proinflammatory genes. Our data confirmed that the effect of hyperthermia as balneological mean treatment is beneficial, but sulfur treatment must be taken in reconsideration.
authors.affiliation: Institute of Medical Biochemistry, Clinical Center of Serbia, Belgrade, Serbia.
authors.forename: Marica
authors.initials: M
authors.lastname: Marković
authors.forename: Nada
authors.initials: N
authors.lastname: Majkić-Singh
authors.forename: Svetlana
authors.initials: S
authors.lastname: Ignjatović
mesh_terms: D001172:Arthritis, Rheumatoid / Q000503:physiopathology / Q000628:therapy*; D001452:Balneology / Q000379:methods*; D001494:Baths / Q000379:methods*; D018932:Chemokine CCL2 / Q000235:genetics; D051546:Cyclooxygenase 2 / Q000235:genetics; D005334:Fever / Q000503:physiopathology; D005347:Fibroblasts / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000517:prevention & control; D053582:Interleukin-1alpha / Q000235:genetics; D053583:Interleukin-1beta / Q000235:genetics / Q000494:pharmacology; D016209:Interleukin-8 / Q000235:genetics; D013455:Sulfur / Q000627:therapeutic use; D013583:Synovial Membrane / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D018932:Chemokine CCL2; D053582:Interleukin-1alpha; D053583:Interleukin-1beta; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D013455:Sulfur; D051546:Cyclooxygenase 2