Neutrophils LL-37 migrate to the nucleus during overwhelming infection.
Pinheiro da Silva. Fabiano F; Medeiros. Maria Cristina Rodrigues MC; Dos Santos. Ângela Batista Gomes ÂB; Ferreira. Marcelo Alves MA; Garippo. Ana Lucia AL; Chammas. Roger R; Caldini. Elia E; Velasco. Irineu Tadeu IT; Possolo de Souza. Heraldo H; Machado. Marcel Cerqueira César MC
Key Findings
- LL‑37 is the only cathelicidin peptide made by human cells and is released by many immune and skin cells.
- During overwhelming infection, LL‑37 was observed to relocate from the outside of the cell into the nucleus.
- The nuclear presence of LL‑37 hints it could affect gene transcription, opening a new line of research.
Practical Outcomes
- At this stage there’s no direct action you can take—no dosage changes or new protocols. The finding is mainly a scientific clue that LL‑37 might have hidden roles inside cells, which could eventually lead to novel health strategies, but more research is needed before it becomes usable for biohackers.
Summary
Scientists found that the immune peptide LL‑37, which normally fights germs outside cells, can actually move into the cell nucleus when the body is fighting a huge infection. This suggests LL‑37 might do more than just kill bacteria, possibly influencing how genes are turned on or off, but we don’t yet know what that means for health or performance.
Abstract
LL-37 is the only cathelicidin produced by human cells. It is secreted by a variety of cell types, including monocyte/macrophages, neutrophils, mast cells, keratinocytes and epithelial cells, acting on the extracellular milieu by directly killing bacteria or boosting innate immunity. Here, we show that LL-37 translocates to the nucleus following overwhelming infection, putting in evidence that its role may be even broader, with new potential important implications to cell biology. Future studies are necessary to address if LL-37 is able to induce or affect transcription, since it can lead to a novel cell signaling pathway that probably will contribute to the understanding of complex diseases.
Study Information
pubmed
2013
2013-06-04T00:00:00.000Z
10.1016/j.tice.2013.04.003
11
30