Title
The antimicrobial peptide LL-37 facilitates the formation of neutrophil extracellular traps
Author
Neumann, A.
Berends, E.T.M.
Nerlich, A.
Molhoek, E.M.
Gallo, R.L.
Meerloo, T.
Nizet, V.
Naim, H.Y.
von Köckritz-Blickwede, M.
Publication year
2014
Abstract
NETs (neutrophil extracellular traps) have been described as a fundamental innate immune defence mechanism. Duringformation of NETs, the nuclear membrane is disrupted by an asyet unknown mechanism. In the present study we investigated the role of human cathelicidin LL-37 in nuclear membrane disruption and formation of NETs. Immunofluorescence microscopy revealed that 5 μMLL-37 significantly facilitated NET formation by primary human blood-derived neutrophils alone, in the presence of the classical chemical NET inducer PMA or in the presence of Staphylococcus aureus. Parallel assays with a random LL-37 fragment library indicated that the NET induction is mediated by the hydrophobic character of the peptide. The translocalization of LL-37 towards the nucleus and the disruption of the nuclear membrane were visualized using confocal fluorescence microscopy. In conclusion, the present study demonstrates a novel role for LL-37 in the formation of NETs.
Subject
Life
CBRN - CBRN Protection
EELS - Earth, Environmental and Life Sciences
Biomedical Innovation
Healthy Living
Cathelicidin
Cell death
Hydrophobicity
NETosis
Neutrophil extracellular trap
Nuclear membrane
Beta defensin 1
Cathelicidin antimicrobial peptide LL 37
Lamin B
Polymyxin B
Animal cell
Bacterial membrane
Cell nucleus membrane
Controlled study
Electron microscopy
Extracellular matrix
Fluorescence microscopy cell
Hydrophobicity
Immunofluorescence microscopy
Male
Mouse
Neutrophil
Neutrophil extracellular trap
Nonhuman
Normal human
Phenotype
Staphylococcus aureus
Polymyxin B, 1404-26-8, 1405-20-5
To reference this document use:
http://resolver.tudelft.nl/uuid:079f5324-ee9a-495d-95fe-f01fb471ab15
DOI
https://doi.org/10.1042/bj20140778
TNO identifier
519653
ISSN
0264-6021
Source
Biochemical Journal, 464, 3-11
Bibliographical note
Funding Details: KO 3552/4-1, DFG, Deutsche Forschungsgemeinschaft
Document type
article