Differential Expression of the <i>apsXRS</i> System by Antimicrobial Peptide LL-37 in Commensal and Clinical <i>Staphylococcus epidermidis</i> Isolates.
Martínez-García. Sergio S; Chávez-Cabrera. Cipriano C; Quintana. Erika T ET; Marsch-Moreno. Rodolfo R; Ibáñez-Hernández. Miguel A MA; Zenteno. Juan Carlos JC; Cruz-Aguilar. Marisa M; Velázquez-Guadarrama. Norma N; Betanzos-Cabrera. Gabriel G; Rodríguez-Martínez. Sandra S; Cancino-Diaz. Mario E ME; Cancino-Diaz. Juan C JC
Key Findings
- All S. epidermidis isolates constantly express the apsXRS system, but LL‑37 boosts its expression 3‑6‑fold only in commensal strains.
- Downstream resistance genes (dlt operon, mprF, vraFG) are 8‑10‑fold more active in commensal isolates after LL‑37 exposure.
- LL‑37 does not cause the bacteria to add lysine to their membrane phospholipids, and no mutations were found in the apsS loop or promoter.
Practical Outcomes
- For DIY health enthusiasts, this research suggests that applying LL‑37 (or LL‑37‑rich products) is unlikely to dramatically alter skin bacterial resistance in a useful way. It highlights that the peptide’s impact on the skin microbiome is strain‑specific and may not translate into a simple antimicrobial boost. No direct dosing or protocol changes are recommended based on these findings.
Summary
The study shows that the human antimicrobial peptide LL‑37 makes harmless skin bacteria (commensal Staphylococcus epidermidis) turn on a defense system more strongly than it does in disease‑linked strains, but this doesn’t change the bacteria’s membrane composition.
Abstract
The three-component <i>apsXRS</i> system senses and responds to cationic antimicrobial peptides (CAMPs), which induces the expression of the <i>dlt</i> operon and the genes <i>mprF</i> and <i>vrafG</i>, modifying the surface net charge in <i>Staphylococcus epidermidis</i>, resulting in the repulsion of CAMPs. The <i>apsXRS</i> system has been only studied in the <i>S. epidermidis</i> 1457 strain, and there are no studies of prevalence and level of expression of <i>apsXRS</i> in commensal and clinical isolates. From 60 isolates, those selected from commensal healthy skin (n = 20), commensal healthy conjunctive (n = 10), and clinical ocular infection (n = 30) presented the <i>apsX</i>, <i>apsR,</i> and <i>apsS</i> genes in their genomes. Constitutive expression of <i>apsX</i>, <i>apsR,</i> and <i>apsS</i> genes was determined by RT-qPCR in all isolates. It was found that expression of <i>apsX</i>, <i>apsR,</i> and <i>apsS</i> was 3.3-5.9-fold higher in commensal isolates stimulated with LL-37 (15 µg/mL) than in clinical isolates. Similarly, expression of the <i>dlt</i> operon and the genes <i>mprF</i>, and <i>vraFG</i> was 8-10-fold higher in commensal isolates than in clinical. However, LL-37 did not increase the addition of lysine in the phospholipids of the cytoplasmic membrane in any of the isolates. Mutations in the <i>apsS</i> loop region, <i>apsR</i>, and their promoter sequence were not found. These results demonstrated that <i>apsXRS</i> system is essential in all isolates for its constitutive expression; however, LL-37 caused an increase of <i>apsXRS</i> expression in commensal isolates, suggesting that <i>S. epidermidis</i> isolates do not respond in the same way to the presence of LL-37.
Study Information
pubmed
2019
2019-04-02T00:00:00.000Z
10.1007/s12088-019-00800-6
6
31