Study summary · research use only
Antimicrobial effects of alpha-MSH peptides
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study examined antimicrobial influences of the anti-inflammatory peptide alpha-melanocyte-stimulating hormone (alpha-MSH (1-13)) and its carboxy-terminal tripeptide (11-13, KPV) against Staphylococcus aureus and the yeast Candida albicans. The authors report that alpha-MSH peptides significantly inhibited S. aureus colony formation, reversed a urokinase-enhanced colony formation, and acted across a broad concentration range including the physiological (picomolar) range. They report reduced viability and germ tube formation in C. albicans, effects they associate with increased cellular cAMP, since an adenylyl cyclase inhibitor partly reversed the killing activity. In assays with human neutrophils, alpha-MSH peptides did not reduce and rather enhanced killing of both pathogens. The authors suggest peptides combining antipyretic, anti-inflammatory, and antimicrobial effects could be useful where infection and inflammation coexist.
Abstract
The presence of the ancient anti-inflammatory peptide alpha-melanocyte-stimulating hormone [alpha-MSH (1-13), SYSMEHFRWGKPV] in barrier organs such as gut and skin suggests a role in the nonspecific (innate) host defense. alpha-MSH and and its carboxy-terminal tripeptide (11-13, KPV) were determined to have antimicrobial influences against two major and representative pathogens: Staphylococcus aureus and Candida albicans. alpha-MSH peptides significantly inhibited S. aureus colony formation and reversed the enhancing effect of urokinase on colony formation. Antimicrobial effects occurred over a broad range of concentrations including the physiological (picomolar) range. Small concentrations of alpha-MSH peptides likewise reduced viability and germ tube formation of the yeast C. albicans. Antimicrobial influences of alpha-MSH peptides could be mediated by their capacity to increase cellular cAMP. Indeed, this messenger was significantly augmented in peptide-treated yeast and the potent adenylyl cyclase inhibitor dideoxyadenosine (ddAdo) partly reversed the killing activity of alpha-MSH peptides. Reduced killing of pathogens is a detrimental consequence of therapy with anti-inflammatory drugs. Because alpha-MSH has potent anti-inflammatory effects we determined influences of alpha-MSH on C. albicans and S. aureus killing by human neutrophils. alpha-MSH peptides did not reduce killing but rather enhanced it, likely as a consequence of the direct antimicrobial activity. alpha-MSH peptides that combine antipyretic, anti-inflammatory, and antimicrobial effects could be useful in treatment of disorders in which infection and inflammation coexist.
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