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LL-37

Cathelicidin, hCAP-18, FALL-39, CAP-18

Quick Stats
Studies 2230
Trials 95
Score 1
2012 pubmed

[Mechanisms of resistance of enterococci to antimicrobial proteins and peptides].

Bukharin. O V OV; Valyshev. A V AV

Key Findings

  • Enterococci modify peptidoglycan and surface charge to resist lysozyme and other peptides
  • The sigma‑factor SigV contributes to resistance mechanisms
  • Enterococci can degrade LL‑37, HNP‑1, cecropin and beta‑lysine, helping them survive in the host

Practical Outcomes

  • For biohackers, the paper suggests that gut Enterococcus may neutralize orally taken LL‑37, so any LL‑37 supplementation could be less effective unless the microbiome is managed. No specific dosing or protocol changes are provided, but it highlights the importance of considering bacterial resistance when experimenting with antimicrobial peptides.

Summary

The review explains how Enterococcus bacteria protect themselves from the body’s natural antimicrobial peptides like LL‑37 by altering their cell wall, changing surface charge, using a special sigma factor, and even breaking down the peptides. This is mainly basic science about bacterial resistance, not a guide for using LL‑37 as a supplement.

Abstract

Mechanisms of resistance of bacteria genus Enterococcus to the most important factors of innate immunity of the host--antimicrobial proteins and peptides--are described in the review. Data on enterococci lysozyme resistance associated with modification of peptidoglycan and changes in the net charge of the bacterial cell surface are presented. The role of enterococci sigma-factor with extra cytoplasmic SigV function is described. Evidence on microbial activation/degradation of neutrophil alpha-defensin (HNP-1), antibacterial peptide LL-37, cecropin, beta-lysine (thrombocytic cationic peptide) is presented. The accumulated experimental material is discussed from the position of persistence of enterococci--both pathogens causing various infectious processes and commensals composing a part of normal host microflora.

Study Information

Provider

pubmed

Year

2012