Legionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles

Abstract Extracellular vesicles from eukaryotic cells and outer membrane vesicles (OMVs) released from gram-negative bacteria have been described as mediators of pathogen-host interaction and intercellular communication. Legionella pneumophila (L. pneumophila) is a causative agent of severe pneumoni...

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Autores principales:	Anna Lena Jung, Christina Elena Herkt, Christine Schulz, Kathrin Bolte, Kerstin Seidel, Nicoletta Scheller, Alexandra Sittka-Stark, Wilhelm Bertrams, Bernd Schmeck
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/634e435cb02945d984a05ad1940c1919
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spelling	oai:doaj.org-article:634e435cb02945d984a05ad1940c19192021-12-02T16:07:06ZLegionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles10.1038/s41598-017-06443-12045-2322https://doaj.org/article/634e435cb02945d984a05ad1940c19192017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06443-1https://doaj.org/toc/2045-2322Abstract Extracellular vesicles from eukaryotic cells and outer membrane vesicles (OMVs) released from gram-negative bacteria have been described as mediators of pathogen-host interaction and intercellular communication. Legionella pneumophila (L. pneumophila) is a causative agent of severe pneumonia. The differential effect of bacterial and host cell vesicles in L. pneumophila infection is unknown so far. We infected THP-1-derived or primary human macrophages with L. pneumophila and isolated supernatant vesicles by differential centrifugation. We observed an increase of exosomes in the 100 k pellet by nanoparticle tracking analysis, electron microscopy, and protein markers. This fraction additionally contained Legionella LPS, indicating also the presence of OMVs. In contrast, vesicles in the 16 k pellet, representing microparticles, decreased during infection. The 100 k vesicle fraction activated uninfected primary human alveolar epithelial cells, A549 cells, and THP-1 cells. Epithelial cell activation was reduced by exosome depletion (anti-CD63, or GW4869), or blocking of IL-1β in the supernatant. In contrast, the response of THP-1 cells to vesicles was reduced by a TLR2-neutralizing antibody, UV-inactivation of bacteria, or – partially – RNase-treatment of vesicles. Taken together, we found that during L. pneumophila infection, neighbouring epithelial cells were predominantly activated by exosomes and cytokines, whereas myeloid cells were activated by bacterial OMVs.Anna Lena JungChristina Elena HerktChristine SchulzKathrin BolteKerstin SeidelNicoletta SchellerAlexandra Sittka-StarkWilhelm BertramsBernd SchmeckNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Anna Lena Jung Christina Elena Herkt Christine Schulz Kathrin Bolte Kerstin Seidel Nicoletta Scheller Alexandra Sittka-Stark Wilhelm Bertrams Bernd Schmeck Legionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles
description	Abstract Extracellular vesicles from eukaryotic cells and outer membrane vesicles (OMVs) released from gram-negative bacteria have been described as mediators of pathogen-host interaction and intercellular communication. Legionella pneumophila (L. pneumophila) is a causative agent of severe pneumonia. The differential effect of bacterial and host cell vesicles in L. pneumophila infection is unknown so far. We infected THP-1-derived or primary human macrophages with L. pneumophila and isolated supernatant vesicles by differential centrifugation. We observed an increase of exosomes in the 100 k pellet by nanoparticle tracking analysis, electron microscopy, and protein markers. This fraction additionally contained Legionella LPS, indicating also the presence of OMVs. In contrast, vesicles in the 16 k pellet, representing microparticles, decreased during infection. The 100 k vesicle fraction activated uninfected primary human alveolar epithelial cells, A549 cells, and THP-1 cells. Epithelial cell activation was reduced by exosome depletion (anti-CD63, or GW4869), or blocking of IL-1β in the supernatant. In contrast, the response of THP-1 cells to vesicles was reduced by a TLR2-neutralizing antibody, UV-inactivation of bacteria, or – partially – RNase-treatment of vesicles. Taken together, we found that during L. pneumophila infection, neighbouring epithelial cells were predominantly activated by exosomes and cytokines, whereas myeloid cells were activated by bacterial OMVs.
format	article
author	Anna Lena Jung Christina Elena Herkt Christine Schulz Kathrin Bolte Kerstin Seidel Nicoletta Scheller Alexandra Sittka-Stark Wilhelm Bertrams Bernd Schmeck
author_facet	Anna Lena Jung Christina Elena Herkt Christine Schulz Kathrin Bolte Kerstin Seidel Nicoletta Scheller Alexandra Sittka-Stark Wilhelm Bertrams Bernd Schmeck
author_sort	Anna Lena Jung
title	Legionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles
title_short	Legionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles
title_full	Legionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles
title_fullStr	Legionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles
title_full_unstemmed	Legionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles
title_sort	legionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/634e435cb02945d984a05ad1940c1919
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Legionella pneumophila infection activates bystander cells differentially by bacterial and host cell vesicles

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