Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection

Abstract Neutrophils represent one of the first immune cell types recruited to sites of infection, where they can control pathogens by phagocytosis and cytotoxic mechanisms. Intracellular pathogens such as Leishmania major can hijack neutrophils to establish an efficient infection. However the dynam...

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Autores principales:	Corinna L. Kleinholz, Monika Riek-Burchardt, Elena A. Seiß, Jonas Amore, Patricia Gintschel, Lars Philipsen, Philippe Bousso, Borna Relja, Burkhart Schraven, Juliane Handschuh, Juliane Mohr, Andreas J. Müller
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f2456a9e704b4f9fa58aa4b2c68737f6
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spelling	oai:doaj.org-article:f2456a9e704b4f9fa58aa4b2c68737f62021-12-02T17:55:04ZLy6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection10.1038/s41598-021-94425-92045-2322https://doaj.org/article/f2456a9e704b4f9fa58aa4b2c68737f62021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94425-9https://doaj.org/toc/2045-2322Abstract Neutrophils represent one of the first immune cell types recruited to sites of infection, where they can control pathogens by phagocytosis and cytotoxic mechanisms. Intracellular pathogens such as Leishmania major can hijack neutrophils to establish an efficient infection. However the dynamic interactions of neutrophils with the pathogen and other cells at the site of the infection are incompletely understood. Here, we have investigated the role of Ly6G, a homolog of the human CD177 protein, which has been shown to interact with cell adhesion molecules, and serves as a bona fide marker for neutrophils in mice. We show that Ly6G deficiency decreases the initial infection rate of neutrophils recruited to the site of infection. Although the uptake of L. major by subsequently recruited monocytes was tightly linked with the concomitant uptake of neutrophil material, this process was not altered by Ly6G deficiency of the neutrophils. Instead, we observed by intravital 2-photon microscopy that Ly6G-deficient neutrophils entered the site of infection with delayed initial recruitment kinetics. Thus, we conclude that by promoting neutrophils’ ability to efficiently enter the site of infection, Ly6G contributes to the early engagement of intracellular pathogens by the immune system.Corinna L. KleinholzMonika Riek-BurchardtElena A. SeißJonas AmorePatricia GintschelLars PhilipsenPhilippe BoussoBorna ReljaBurkhart SchravenJuliane HandschuhJuliane MohrAndreas J. MüllerNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Corinna L. Kleinholz Monika Riek-Burchardt Elena A. Seiß Jonas Amore Patricia Gintschel Lars Philipsen Philippe Bousso Borna Relja Burkhart Schraven Juliane Handschuh Juliane Mohr Andreas J. Müller Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection
description	Abstract Neutrophils represent one of the first immune cell types recruited to sites of infection, where they can control pathogens by phagocytosis and cytotoxic mechanisms. Intracellular pathogens such as Leishmania major can hijack neutrophils to establish an efficient infection. However the dynamic interactions of neutrophils with the pathogen and other cells at the site of the infection are incompletely understood. Here, we have investigated the role of Ly6G, a homolog of the human CD177 protein, which has been shown to interact with cell adhesion molecules, and serves as a bona fide marker for neutrophils in mice. We show that Ly6G deficiency decreases the initial infection rate of neutrophils recruited to the site of infection. Although the uptake of L. major by subsequently recruited monocytes was tightly linked with the concomitant uptake of neutrophil material, this process was not altered by Ly6G deficiency of the neutrophils. Instead, we observed by intravital 2-photon microscopy that Ly6G-deficient neutrophils entered the site of infection with delayed initial recruitment kinetics. Thus, we conclude that by promoting neutrophils’ ability to efficiently enter the site of infection, Ly6G contributes to the early engagement of intracellular pathogens by the immune system.
format	article
author	Corinna L. Kleinholz Monika Riek-Burchardt Elena A. Seiß Jonas Amore Patricia Gintschel Lars Philipsen Philippe Bousso Borna Relja Burkhart Schraven Juliane Handschuh Juliane Mohr Andreas J. Müller
author_facet	Corinna L. Kleinholz Monika Riek-Burchardt Elena A. Seiß Jonas Amore Patricia Gintschel Lars Philipsen Philippe Bousso Borna Relja Burkhart Schraven Juliane Handschuh Juliane Mohr Andreas J. Müller
author_sort	Corinna L. Kleinholz
title	Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection
title_short	Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection
title_full	Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection
title_fullStr	Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection
title_full_unstemmed	Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection
title_sort	ly6g deficiency alters the dynamics of neutrophil recruitment and pathogen capture during leishmania major skin infection
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/f2456a9e704b4f9fa58aa4b2c68737f6
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Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection

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