Antimicrobial peptides in the pathogenesis of psoriasis.
Morizane. Shin S; Gallo. Richard L RL
Key Findings
- LL‑37 levels are elevated in psoriatic skin lesions
- LL‑37 can both worsen and potentially improve psoriasis by affecting the immune system
- More research is needed before LL‑37 can be targeted safely in humans
Practical Outcomes
- At present there’s no actionable protocol for biohackers; the finding mainly points to LL‑37 as a future drug target, so it’s more of a research interest than a practical tool for longevity or performance.
Summary
The study explains that a small protein called LL‑37 is found in high amounts in the skin of people with psoriasis and can influence inflammation, but it doesn’t give any clear ways to use this information for health hacks or treatments right now.
Abstract
One characteristic abnormality of lesional skin in psoriasis is the excessive production of antimicrobial peptides and proteins (AMPs). AMPs typically are small (12-50 amino acids), have positive charge and amphipathic structure, and are found in all living organisms including mammals, insects, plants and invertebrates. These peptides are best known for their integral role in killing pathogenic microorganisms; however, in vertebrates, they are also capable of modifying host inflammatory responses by a variety of mechanisms. In psoriatic lesions, many AMPs are highly expressed, and especially the associations between psoriasis and cathelicidin, β-defensins or S100 proteins have been well studied. Among them, a cathelicidin peptide, LL-37, has been highlighted as a modulator of psoriasis development in recent years. AMPs had been thought to worsen psoriatic lesions but recent evidence has also suggested the possibility that the induction of AMPs expression might improve aspects of the disease. Further investigations are needed to uncover a previously underappreciated role for AMPs in modulating the immune response in psoriasis, and to improve disease without the risks of systemic immunosuppressive approaches.
Study Information
pubmed
2012
2012-03-01T00:00:00.000Z
10.1111/j.1346-8138.2011.01483.x
233
83