Study summary · research use only
The neuroimmunomodulatory peptide alpha-MSH
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses alpha-melanocyte-stimulating hormone (alpha-MSH), described as a neuroimmunomodulatory peptide involved in host inflammatory responses; species not specified. The authors describe alpha-MSH as modulating production and action of proinflammatory cytokines in inflammatory cells both peripherally and within the central nervous system, acting through melanocortin receptors, with the anti-inflammatory action attributed to inhibition of NF-kappa B via preservation of I kappa B alpha. Cells transfected with an alpha-MSH plasmid vector were reported to resist challenge with bacterial lipopolysaccharide. The review describes alpha-MSH and fragments such as alpha-MSH [11-13] KPV as acting through direct effects on peripheral host cells, effects on inflammatory cells within the brain, and descending neural pathways that modulate peripheral inflammation.
Abstract
Alpha-melanocyte-stimulating hormone (alpha-MSH), a neuroimmunomodulatory peptide of ancient origin, is known to be involved in the control of host responses. In inflammatory cells, in the periphery and within the central nervous system, alpha-MSH modulates the production and action of proinflammatory cytokines. This broad influence occurs via endogenous alpha-MSH (melanocortin) receptors. The key to this anti-inflammatory influence is inhibition of NF-kappa B. Indeed alpha-MSH inhibits activation of this nuclear factor through preservation of I kappa B alpha, which binds to NF-kappa B and prevents its migration to the nucleus. Cells transfected with alpha-MSH plasmid vector are resistant to challenge with bacterial lipopolysaccharide. The peptide also act on central melanocortin receptors to modulate inflammation in the periphery. In brief, alpha-MSH and certain of its fragments such as alpha-MSH [11-13] KPV modulate inflammation via three general actions: direct actions on peripheral host cells; actions on inflammatory cells within the brain to modulate local reactions; and descending neural anti-inflammatory pathways that control inflammation in peripheral tissues.
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