The role of Staphylococcal carotenogenesis in resistance to host defense peptides and in vivo virulence in experimental endocarditis model.
Xiong. Yan Q YQ; Yang. Soo-Jin SJ; Tong. Steven Y C SY; Alvarez. Danya N DN; Mishra. Nagendra N NN
Key Findings
- Carotenoid complementation restores pigment production and increases membrane rigidity in Staphylococcus argenteus strains.
- Pigmented, membrane‑rigid bacteria become more susceptible to the host defense peptide LL‑37 and hNP‑1 in vitro.
- In a rabbit endocarditis model, carotenoid‑producing bacteria show reduced virulence compared to non‑pigmented controls.
Practical Outcomes
- For the biohacker community, the study highlights that bacterial membrane composition can influence how well LL‑37 works, but it does not provide any new dosing guidelines or direct health interventions. No immediate actionable steps for personal use of LL‑37 are suggested.
Summary
Adding the pigment‑making genes to a normally non‑pigmented Staph strain made the bacteria produce a carotenoid and stiffen their cell walls, but surprisingly this also made them easier for the natural antimicrobial peptide LL‑37 (and hNP‑1) to kill, and they caused less severe heart infections in rabbits. The work is mainly about bacterial genetics and infection, not about how people can use LL‑37 for health.
Abstract
The defining hallmark of the newly described species, Staphylococcus argenteus, in comparison to its sister species, S. aureus and S. schweitzeri, is the absence of production of the carotenoid pigment, staphyloxanthin. Staphylococcus argenteus lacks the responsible genetic locus crtOPQMN. We examined the impact of carotenoid synthesis in two non-pigmented S. argenteus strains, MSHR1132 and SCC1165. Following complementation with a plasmid containing the carotenoid operon (pTX-crtOPQMN), compared to wild type, both complemented strains showed substantial carotenoid production, with a resultant increase in cell membrane rigidity. Surprisingly, both crtOPQMN-complemented strains exhibited increased susceptibility to the host defense peptides, LL-37 and hNP-1 in vitro, and reduced virulence in an experimental rabbit endocarditis model.
Study Information
pubmed
2015
2015-08-04T00:00:00.000Z
10.1093/femspd/ftv056
15
21