Cytokine profile of Armenian patients with Familial Mediterranean fever.

OBJECTIVES: Despite the well-defined genetics of FMF, limited information is available regarding the regulation of inflammation by cytokines. DESIGN AND METHODS: The levels of systemic cytokines and other markers of inflammation in FMF patients and control were measured by ELISA and Cytometric Bead Array (CBA). RESULTS: In FMF attack the levels of IL-6, IL-10, IL-17, TGF-beta, CRP, and sIL-2R were significantly different from the norm and FMF remission. CONCLUSIONS: Inflammation in FMF involves Treg and Th17 lineages.

Engaging anti-inflammatory mechanisms and triggering inflammatory effector apoptosis during Familial Mediterranean Fever attack.

OBJECTIVE: To investigate endotoxin-induced tolerance, intracellular cytokine synthesis polarization and monocyte apoptosis during Familial Mediterranean Fever (FMF). METHODS: Lipopolysaccharide (LPS)-induced tolerance, intracellular cytokine synthesis and monocyte apoptosis were determined in FMF patients by flow cytometry using whole blood cell culture technique. RESULTS: Endotoxin homo- and cross-tolerance, detected as the percentage of TNF-alpha synthesizing monocytes, developed in whole blood preparations of patients in attack period, but not during remission. The induction of anti-inflammatory cytokine synthesis polarization and enhancement of iodine-lithium-alpha-dextrin- and LPS-induced monocyte apoptosis was observed in FMF patients during the attack, whereas monocytes from patients in remission period exhibited proinflammatory cytokine polarization and resistance to the repeated LPS-induced apoptosis. Colchicine induced anti-inflammatory cytokine synthesis and caused down-modulation of monocyte apoptosis, whereas cytokines did not alter LPS-induced monocyte apoptosis. CONCLUSION: The self-limited nature of attacks during FMF may represent periods of inflammation resolution compensatory to continued sub-clinical inflammation during the remission.