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Spinal 'Cross-Talk' May Play Role in Arthritis Spread

Mouse studies focus on inflammatory mediator interleukin 1-β in joint pathology and pain

WEDNESDAY, Oct. 1 (HealthDay News) -- Bidirectional cross-talk between the body's periphery and the central nervous system may help arthritis transmit inflammation to the spinal cord, where it may spread arthritis to other joints, according to research published online Sept. 29 in Arthritis & Rheumatism.

Paolo M. Fiorentino, of the University of Rochester School of Medicine and Dentistry in Rochester, N.Y., and colleagues discuss the results of several experiments on mice. They found that increasing interleukin 1-β (IL-1β) in a peripheral joint led to elevated levels of IL-1β in the dorsal horns of the spinal cord. The investigators also found that disrupting or intrathecally inhibiting the IL1β-IL1RI signaling pathway significantly reduced the degree of arthritis in mice.

Furthermore, the researchers found that activating the IL1β-IL1RI signaling pathway in the spinal cord is sufficient for creating neuroinflammatory, sensory and behavioral changes in mice.

"Our studies demonstrate that IL-1β in the dorsal horns, regardless of its exact cell origin (neurons, astrocytes), is both contributory and sufficient for the development of arthritis. Furthermore, a possible role of astroglia in the development of nociceptive behavior and joint pathology through cell-cell (astroglia-neuron) interactions is suggested. To our knowledge, ours is the first report indicating that dorsal horn astrocytes can influence peripheral disease development," the authors write. "The proposed central nervous system-periphery cross-talk is likely to play a critical role in the expansion and exacerbation of peripheral tissue pathology along with the expansion of nociceptive fields, and provides a new area for therapeutic intervention."

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