An antibiotic created from human sweat might fight off hospital superbugs and deadly strains of tuberculosis, scientists reported in Proceedings of the National Academy of Sciences.
The researchers, from Scotland, Germany, France and Spain explained that a protein found on human skin – Dermcidin – is activated in sweat (slightly acidic and salty environments) and kills harmful microbes by perforating their cell membranes.
Dermcidin is a natural protein, part of our natural defences, that is present on our skin when we sweat. The authors wrote that understanding how these natural defences work could help researchers design effective alternatives to conventional antibiotic medications.
Until now, the scientific community could not fully explain how proteins produced by animals and plants have been fending off harmful bacteria, viruses and funguses for millions of years.
If we can eventually unravel how proteins such as dermcidin work, we may be better equipped to fight off infections which are becoming progressively more resistant to all our current antibiotics, such as MRSA (Methicillin-resistant Staphylococcus aureus).
Dr Ulrich Zachariae, from the University of Edinburgh, and colleagues set out to study infection-fighting proteins produced by sweat glands and on human skin.
They discovered that these proteins are shaped like a pipe by observing them with specialist X-ray imaging technology.
The protein molecule can push fluids through its pipe-structure to rupture the membranes of microbes, destroying them in fractions of a second. Dermcidin can adapt to different types of membranes, allowing it to fight off bacteria and fungi simultaneously.
Apart from being active against the hospital superbug Staphylococcus aureus, dermcidin destroys Mycobacterium tuberculosis and tuberculosis.
These bug-fighting molecules, known as AMPs (antimicrobial peptides) are much more effective in the long-term than the current antibiotics used in hospitals, because microbes cannot develop resistance against them rapidly. They attack the microbe’s “Achilles heel”, its cell wall, which cannot adapt quickly to resist attack.
If scientists could design antibiotics to mimic what dermcidin does, we may well be able to develop better drug therapies for resistant infections.
Written by Christian Nordqvist