Eriksson Per, Andersson Carina, Ekerfelt Christina, Ernerudh Jan, Skogh Thomas
Division of Rheumatology, Department of Molecular and Clinical Medicine, Autoimmunity and Immunoregulation Unit, Faculty of Health Sciences, Linköping University Hospital, Linköping, Sweden.
J Rheumatol. 2004 Apr;31(4):729-35.
To measure in vitro cytokine release from peripheral blood mononuclear cells (PBMC) and serum cytokines in patients with primary Sjögren's syndrome (SS) with and without myalgia, compared to patients with rheumatoid arthritis (RA) and healthy controls.
Sixteen women with SS (8 with myalgia, 8 without pain), 15 women with RA, and 14 healthy women were studied. PBMC were isolated and cultured. Secretion of interleukin 1 beta (IL-1 beta), IL-6, IL-10, and tumor necrosis factor-alpha (TNF-alpha) was measured in cell supernatants with or without stimulation with phytohemagglutinin, tetanus toxoid, or purified protein derivative (PPD). Enzyme-linked immunospot was used to enumerate interferon-gamma (IFN-gamma) and IL-4-secreting cells. Serum concentrations of IL-8 and IL-18 were analyzed by ELISA.
PPD-stimulated PBMC from SS patients responded with less production of IL-10, TNF-alpha, and IFN-gamma compared to controls. Patients with SS and pain were hyporesponsive also with respect to IL-1 beta and IL-6. The generally subnormal cytokine release was statistically significant in myalgic patients with SS compared to healthy controls. Serum IL-18 was increased in both SS groups as well as in patients with RA, and the highest levels were found in myalgic patients with SS. Serum IL-8 was increased in RA but not in SS.
Patients with SS, especially those with myalgia, had diminished PBMC cytokine release and increased serum IL-18. This finding suggests that impaired cytokine regulation may have pathogenetic importance for myalgia in SS.
