Evaluation of plasma antimicrobial peptide LL-37 and nuclear factor-kappaB levels in stable chronic obstructive pulmonary disease.
Uysal. Pelin P; Simsek. Gonul G; Durmus. Sinem S; Sozer. Volkan V; Aksan. Hulya H; Yurt. Sibel S; Cuhadaroglu. Caglar C; Kosar. Filiz F; Gelisgen. Remise R; Uzun. Hafize H
Key Findings
- COPD patients have significantly reduced plasma LL‑37 compared to healthy controls.
- Plasma NF‑κB levels are markedly increased in COPD patients, especially in advanced stages.
- LL‑37 and NF‑κB levels are inversely correlated; lower LL‑37 associates with higher NF‑κB and worse lung function.
Practical Outcomes
- For biohackers, this study suggests that maintaining or boosting LL‑37 could theoretically help dampen chronic lung inflammation, but no supplementation or dosing protocol is provided. Until intervention trials emerge, the main actionable insight is to monitor emerging research on LL‑37‑targeted therapies or lifestyle factors that might support innate immunity.
Summary
In people with stable COPD, blood levels of the immune peptide LL‑37 are lower while the inflammation driver NF‑κB is higher, especially in the most severe disease stage. The two markers are inversely linked, meaning when LL‑37 drops, NF‑κB rises, and lower LL‑37 is tied to poorer lung function.
Abstract
Antimicrobial peptides are effectors of host defence against infection and inflammation and can encourage wound repair. The objectives of this study were to investigate the plasma antimicrobial peptide LL-37 and nuclear factor-kappaB (NF-κB) levels in patients with stable COPD compared with a control group and to highlight their importance in immune inflammation. One hundred and thirty-eight stable COPD patients and 33 control subjects were enrolled in the study. The COPD patients were classified into four groups based on FEV<sub>1</sub> (groups I-IV) and also divided into "low-risk and high-risk" groups (groups A-B [low risk], C-D [high risk]). Plasma LL-37 levels were significantly lower while plasma NF-κB levels of the COPD patients were significantly higher than those of the control subjects (<i>P</i><0.001, both). LL-37 levels were significantly lower in group IV than in groups I, II, and III (<i>P</i><0.01, all). NF-κB levels were significantly higher in groups III and IV than in groups I and II (<i>P</i><0.05, both). There was a positive correlation between FEV<sub>1</sub> and FEV<sub>1</sub>/FVC in all COPD patients (<i>r</i>=0.742, <i>P</i><0.001) and in group D (<i>r</i>=0.741, <i>P</i><0.001). Furthermore, there was an inverse correlation between LL-37 and NF-κB in both the groups C (<i>r</i>=-0.566, <i>P</i><0.001) and D (<i>r</i>=-0.694, <i>P</i><0.001) and group C+D combined (<i>r</i>=-0.593, <i>P</i><0.001). Furthermore, in group C, LL-37 and FEV<sub>1</sub> were positively correlated (<i>r</i>=0.633, <i>P</i><0.001). Our study indicated that plasma LL-37 and NF-κB may play an important role in chronic immune inflammation. Decreased LL-37 levels may be particularly high risk for patients in stage IV disease. The role of LL-37 as a target for treatment of the immune system and COPD must be widely evaluated.
Study Information
pubmed
2019
2019-01-25T00:00:00.000Z
10.2147/copd.s185602