Human-derived cathelicidin LL-37 directly activates mast cells to proinflammatory mediator synthesis and migratory response.
Bąbolewska. Edyta E; Brzezińska-Błaszczyk. Ewa E
Key Findings
- LL-37 directly causes mast cell degranulation and release of certain pro‑inflammatory cytokines.
- LL-37 does not induce cysteinyl leukotriene production in mast cells.
- LL-37 acts as a strong chemoattractant for mast cells, drawing them to the site of exposure.
- The signaling pathways involved include PLC/A2, MAPKs (partially), and PI3K.
Practical Outcomes
- LL-37 might be useful for quickly rallying immune cells against infections, but it also provokes inflammation, so using it as a supplement could have unwanted side effects. Without clear safety and dosing data, biohackers should be cautious and wait for more research before adding LL-37 to health protocols.
Summary
The study shows that the human peptide LL-37 can directly fire up mast cells, causing them to release some inflammatory chemicals and move toward the site, but it doesn't trigger all the usual inflammatory pathways. This suggests LL-37 can boost early immune defenses, but it also raises inflammation, and the research doesn’t give any guidance on safe dosing for everyday use.
Abstract
Cathelicidins, a family of antimicrobial peptides, are well known for their role in host defense, particularly against bacteria. Apart from direct killing of microbes through the membrane disruption, cathelicidins can also exert immunomodulatory effects on cells involved in inflammatory processes. Considering the important role of mast cells in inflammation, the aim of this study was to determine whether LL-37, human-derived cathelicidin, can induce mast cell activation. We have observed that LL-37 directly stimulates mast cell to degranulation and production of some proinflammatory cytokines, but fails to induce cysteinyl leukotriene generation and release. We have also documented that LL-37 acts as a strong mast cell chemoattractant. In intracellular signaling in mast cells activated by LL-37 participates PLC/A2 and, in part, MAPKs, and PI3K. In conclusion, our results indicate that cathelicidins may enhance antibacterial inflammatory response via attracting mast cell to pathogen entry site and via induction of mast cell-derived mediator release.
Study Information
pubmed
2015
2015-01-03T00:00:00.000Z
10.1016/j.cellimm.2014.12.006
50
42