Gewählte Publikation:
SHR
Neuro
Krebs
Kardio
Lipid
Stoffw
Microb
Rani, A; Balandin, D; Ravi, R; Teppan, J; Vidakovic, I; Kienzl, M; Bärnthaler, T; Holzer, M; Zijadic, L; Heinemann, A; Jandl, K; Böhm, E; Kornmueller, K; Tarek, M; Prassl, R; Marsche, G.
Peptide-based lipid nanodiscs suppress eosinophil recruitment and chemotaxis.
J Control Release. 2025; 114060
Doi: 10.1016/j.jconrel.2025.114060
PubMed
FullText
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- Führende Autor*innen der Med Uni Graz
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Marsche Gunther
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RANI Alankrita
- Co-Autor*innen der Med Uni Graz
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Balandin Denys
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Bärnthaler Thomas
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Böhm Eva
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Heinemann Akos
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Holzer Michael
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Jandl Katharina
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Kienzl Melanie
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Kornmüller Karin
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Prassl Ruth
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Teppan Julia
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Vidakovic Ivan
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Zijadic Lamija
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- Abstract:
- Apolipoprotein A-I (ApoA-I) mimetic peptides hold promise for treating inflammatory lung diseases, yet their impact on eosinophils, key mediators of asthma and allergic airway inflammation, remains underexplored. We prepared self-assembling synthetic high-density lipoprotein (sHDL) nanoparticles using the bihelical ApoA-I mimetic peptide 4F-P-4F and phospholipids via microfluidics, yielding stable, nanodisc-shaped structures, as confirmed by in vitro and in silico analyses. These sHDL nanoparticles potently inhibited eotaxin-induced eosinophil migration in vitro, an effect reversed by blocking HDL receptors SR-BI and ABCA1. Mechanistically, sHDL promoted cholesterol efflux, disrupted CCR3 internalization, and modulated ERK1/2, STAT1, and STAT3 signaling. In an IL-5 transgenic mouse model, sHDL significantly reduced eosinophil infiltration in bronchoalveolar lavage. These results show that sHDL nanoparticles suppress eosinophil migration through targeted receptor interactions and signaling modulation, providing a mechanistic basis for further drug development.