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Melanocortin peptides inhibit urate crystal-induced activation of phagocytic cells
Arthritis Research & Therapy, 10/12/09

Capsoni F et al. – alpha-MSH and (CKPV)2 have a dual effect on MSU crystal-induced inflammation, inhibiting the Mo's ability to produce neutrophil chemoattractants and activating compounds and preventing the neutrophil responses to these pro-inflammatory substances. These findings reinforce previous observations on the potential role of alpha-MSH and related peptides as a new class of drugs for treatment of inflammatory arthritis.

Methods

Purified monocytes (Mo) stimulated with monosodium urate (MSU) crystals in presence or absence of melanocortin peptides
The supernatants were tested for ability to induce neutrophil activation in terms of chemotaxis, production of reactive oxygen intermediates (ROI), and membrane expression of CD11b, Toll-like receptor (TLR)2 and TLR4
Pro-inflammatory cytokines interleukin (IL)-1beta, IL-8, and tumor necrosis factor (TNF)-alpha and caspase-1 determined in cell-free supernatants
In parallel experiments, purified neutrophils were preincubated overnight with or without melanocortin peptides before the functional assays

Results

Supernatants from MSU crystal-stimulated Mo exerted chemoattractant and priming activity on neutrophils, estimated as ROI production and CD11b membrane expression
Supernatants of Mo stimulated with MSU in presence of melanocortin peptides had less chemoattractant activity for neutrophils and less ability to prime neutrophils for CD11b membrane expression and oxidative burst
MSU crystal-stimulated Mo produced significant levels of IL-1beta, IL-8, TNF-alpha and caspase-1
Concentrations of pro-inflammatory cytokines reduced in supernatants from Mo stimulated by MSU crystals in presence of melanocortin peptides
Overnight incubation of neutrophils with peptides significantly inhibited their ability to migrate toward chemotactic supernatants and capacity to be primed in terms of ROI production

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