Study summary · research use only
Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study using a mouse model of crystal-induced peritonitis, the authors compared systemic treatment with the C-terminal alpha-MSH tripeptide KPV, alpha-MSH, the core melanocortin peptide His-Phe-Arg-Trp, and the MC3/4-receptor agonist MTII, versus a selective MC1-R agonist (MS05). They reported that KPV, alpha-MSH, the core peptide, and MTII, but not MS05, were associated with reduced accumulation of polymorphonuclear leukocytes in the peritoneal cavity, and that KPV's antimigratory action was not blocked by the MC3/4-R antagonist SHU9119. In vitro, alpha-MSH and MTII, but not KPV, inhibited macrophage release of KC and IL-1beta; MTII increased cAMP accumulation, attenuated by SHU9119, while KPV did not increase cAMP. The authors concluded KPV's anti-inflammatory action differs from that of the core MSH peptides and likely does not act through melanocortin receptors.
Abstract
In this study, we analyzed the anti-inflammatory effects of alpha-melanocyte stimulating hormone (MSH)11-13 (KPV) in comparison with other MSH peptides in a model of crystal-induced peritonitis. Systemic treatment of mice with KPV, alpha-MSH, the core melanocortin peptide His-Phe-Arg-Trp, and the melanocontin receptor 3/4 agonist Ac-Nle4-c[Asp5,d-Phe7,Lys10]NH2 ACTH4-10 (MTII) but not the selective MC1-R agonist H-Ser-Ser-Ile-Ile-Ser-His-Phe-Arg-Trp-Gly-Lys-Pro-Val-NH2 (MS05) resulted in a significant reduction in accumulation of polymorphonuclear leukocyte in the peritoneal cavity. The antimigratory effect of KPV was not blocked by the MC3/4-R antagonist Ac-Nle4-c[Asp5,d-2Nal7,Lys10]NH2 ACTH4-10 (SHU9119). In vitro, macrophage activation, determined as release of KC and interleukin (IL)-1beta was inhibited by alpha-MSH and MTII but not by KPV. Furthermore, macrophage activation by MTII led to an increase in cAMP accumulation, which was attenuated by SHU9119, whereas KPV failed to increase cAMP. The anti-inflammatory properties of KPV were also evident in IL-1beta-induced peritonitis inflammation and in mice with a nonfunctional MC1-R (recessive yellow e/e mice). In conclusion, these data highlight that the C-terminal MSH peptide KPV exhibits an anti-inflammatory effect that is clearly different from that of the core MSH peptides. KPV is unlikely to mediate its effects through melanocortin receptors but is more likely to act through inhibition of IL-1beta functions.
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