Antimicrobial peptide LL-37 attenuates LTA induced inflammatory effect in macrophages.
Ruan. Yang Y; Shen. Tao T; Wang. Yan Y; Hou. Man M; Li. Jian J; Sun. Tieying T
Key Findings
- LL‑37 levels rise when cells are exposed to LTA
- LL‑37 blocks p38MAPK and Akt activation triggered by LTA
- LL‑37 reduces the release of TNF‑α and IL‑6 from macrophages
Practical Outcomes
- LL‑37 appears to have anti‑inflammatory properties, suggesting it could be explored as a supplement or therapeutic agent for reducing bacterial‑induced inflammation. However, the study provides no dosage guidelines or delivery methods, so biohackers would need to await further research before practical use.
Summary
The study shows that the human peptide LL‑37 can calm down inflammation caused by a bacterial component (LTA) in immune cells by blocking certain signaling pathways and lowering inflammatory chemicals like TNF‑α and IL‑6.
Abstract
LL-37/hCAP-18, as the only human cathelicidin, plays an important role in inflammation. Lipoteichoic acid (LTA) is an important bacterial component of Staphylococcus aureus, which is one of the common human pathogens for severe respiratory infection with increasing morbidity in recent years. The present study is to investigate the role of LL-37 in LTA induced inflammatory reaction in macrophages. We examined TNF-α and IL-6 production after LL-37 treatment and discussed its signal transduction pathways such as p38MAPK and Akt activation in macrophages. The expression of pro-inflammatory cytokines was analyzed by quantitative real-time RT-PCR and enzyme-linked immunosorbent assay (ELISA). The LL-37 expression was determined by Western blot and immunofluorescence staining. The results showed that LL-37 was upregulated after LTA treatment. It could inhibit LTA induced p38MAPK and Akt phosphorylation and attenuate TNF-α and IL-6 production in macrophages in some specific concentration. These results suggest that LL-37 exerts an anti-inflammatory property and attenuates the pro-inflammatory cytokine release in macrophages.
Study Information
pubmed
2013
2013-01-29T00:00:00.000Z
10.1016/j.intimp.2013.01.012
48
28