ArticleMedical science monitor : international medical journal of experimental and clinical research2019
LL-37 Exacerbates Local Inflammation in Sepsis-Induced Acute Lung Injury by Preventing Mitochondrial DNA (mtDNA) Degradation-Induced Autophagy.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- New trends and hotspots in sepsis-related protein post-translational modification: a bibliometric and visual analysis.Frontiers in medicine · 2025Pooled it
- Downregulation of IGFBP7 Alleviates LPS-induced Inflammation and Apoptosis in WI-38 Cells via Enhancing Mitophagy.Cell biochemistry and biophysics · 2025Article
- Between good and evil: Complexation of the human cathelicidin LL-37 with nucleic acids.Biophysical journal · 2024Review
- LL37-mtDNA regulates viability, apoptosis, inflammation, and autophagy in lipopolysaccharide-treated RLE-6TN cells by targeting Hsp90aa1.Open life sciences · 2024Article
- Role and mechanisms of autophagy, ferroptosis, and pyroptosis in sepsis-induced acute lung injury.Frontiers in pharmacology · 2024Review
- MiRNAs and Neutrophil-Related Membrane Proteins from Plasma-Derived Extracellular Vesicles for Early Prediction of Organ Dysfunction and Prognosis in Septic Patients.Journal of inflammation research · 2024Article
- Role of LL-37 in thrombotic complications in patients with COVID-19.Cellular and molecular life sciences : CMLS · 2022Article
- Dysregulation of neutrophil death in sepsis.Frontiers in immunology · 2022Review
- [Effect of mogroside VI on acute liver injury induced by sepsis in mice and related mechanisms].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2020Article
- Diagnostic value of miR-155 for acute lung injury/acute respiratory distress syndrome in patients with sepsis.The Journal of international medical research · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Recent studies have proved that autophagy dysfunction in proinflammatory cells is involved in tissue damage and an excessive inflammatory response in sepsis. In the present study, we identified that the human antimicrobial peptide LL-37 facilitates resistance to DNase II-induced mitochondrial DNA (mtDNA) degradation and subsequent autophagy. MATERIAL AND METHODS We found higher serum levels of LL-37 in patients with severe sepsis compared to that in patients with mild sepsis. Neutrophils isolated from mice with sepsis after treatment with Cramp-mtDNA produced an excess of proinflammatory cytokines, including IL-1ß, IL-6, IL-8, MMP-8, and TNF-alpha. Cramp-mtDNA in the lung samples from model animals with sepsis was detected by immunohistochemical staining. RESULTS Exogenous delivery of Cramp-mtDNA complex significantly exacerbated lung inflammation but the antibody against Cramp-mtDNA attenuated the excessive inflammatory response in LPS-induced acute lung injury. The expression of proinflammatory cytokines in lungs was upregulated and downregulated after treatment with the complex and antibody, respectively. LC-3 expression in 16HBE cells increased after LPS induction, irrespective of stimulation with LL-37. CONCLUSIONS These data show that LL-37 treatment worsens local inflammation in sepsis-induced acute lung injury by preventing mtDNA degradation-induced autophagy.
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