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Staphylococcus epidermidis isolated from newborn infants express pilus-like structures and are inhibited by the

Annika Nelson1, Kjell Hultenby, Eva Hell

  • 1Department of Woman and Child Health, Karolinska Institutet, Stockholm 17176, Sweden.

Pediatric Research
|April 25, 2009
PubMed

Insights

Newborn skin harbors Staphylococcus epidermidis, a common bacteria. The study found antimicrobial peptide LL37 inhibits S. epidermidis growth, highlighting its role in infant skin immunity and microbial balance.

Area of Science:

  • Microbiology
  • Immunology
  • Dermatology

Background:

  • Coagulase-negative staphylococci, particularly Staphylococcus epidermidis, are key Gram-positive bacteria colonizing human skin from birth.
  • The skin's barrier function, crucial for defense, involves antimicrobial peptides like human cathelicidin LL37.
  • Gram-positive bacteria possess pili for host attachment, influencing colonization dynamics.

Purpose of the Study:

  • To investigate factors influencing newborn skin colonization by S. epidermidis.
  • To characterize pilus-like structures on S. epidermidis relevant to infant skin.
  • To assess the impact of the antimicrobial peptide LL37 on S. epidermidis growth in the context of infant skin immunity.

Main Methods:

  • Negative staining transmission electron microscopy (EM) to visualize bacterial structures.
  • Isolation and culture of S. epidermidis from newborn infants.
  • Growth inhibition assays using the antimicrobial peptide LL37.

Main Results:

  • Two distinct types of pilus-like structures were identified on S. epidermidis strains from newborns.
  • The antimicrobial peptide LL37 significantly inhibited the growth of S. epidermidis.
  • LL37 demonstrates a role in maintaining the ecological stability of the neonatal skin microbiota.

Conclusions:

  • S. epidermidis possesses unique pilus structures potentially involved in infant skin colonization.
  • The innate immune component LL37 plays a critical role in regulating S. epidermidis on newborn skin.
  • Further research is needed to understand host-microbe interactions for maintaining skin homeostasis and preventing disease.

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