Peptide directorySkin, immune & repair

Human beta-defensin 3

The most potent beta-defensin, which kills staphylococci in salt where others fail.

Where it comes from

Made in
Keratinocytes, tonsil, airway, gingiva and placenta, induced by injury and infection
Sent out by
Wounding, bacteria and interferon-gamma switch it on
Acts on
  • Staphylococcus aureus including MRSA
  • Streptococci
  • Candida
  • HIV

What it does

  • Kills Gram-positive bacteria at physiological salt, which most defensins cannot
  • Blocks lipid II, the cell-wall building block, as vancomycin does
  • Binds the melanocortin receptor MC1R, which in dogs sets coat colour

In medicine

  • No medicine; copy number of its gene pair varies between people and is studied in psoriasis and Crohn’s disease 4
  • It is the human defensin that keeps killing Staphylococcus aureus at the salt of body fluid, which is why antibacterial work starts here 1

Beyond the body’s own use

  • It blocks lipid II, the cell-wall building block vancomycin binds, so it is studied as a template for antibiotics against resistant Gram-positive bacteria 2
  • Engineered versions are tested on skin and implant infections in animals; none has reached a human trial
  • The dog version of this gene sets black coat colour through the melanocortin receptor, the clearest evidence that a defensin can double as a pigment signal 3

Sources

  1. Harder et al., Isolation and characterization of human beta-defensin-3, Journal of Biological Chemistry 2001
  2. Sass et al., Human beta-defensin 3 inhibits cell wall biosynthesis in staphylococci, Infection and Immunity 2010
  3. Candille et al., A beta-defensin mutation causes black coat colour in domestic dogs, Science 2007
  4. Hollox et al., Psoriasis is associated with increased beta-defensin genomic copy number, Nature Genetics 2008

This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.