Cargando…

Type I IFN suppresses Cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection

Infection induces the expression of inflammatory chemokines that recruit immune cells to the site of inflammation. Whereas tissues such as the intestine and skin express unique chemokines during homeostasis, whether different tissues express distinct chemokine profiles during inflammation remains un...

Descripción completa

Detalles Bibliográficos
Autores principales: Stock, Angus T., Smith, Jeffrey M., Carbone, Francis R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4010892/
https://www.ncbi.nlm.nih.gov/pubmed/24752295
http://dx.doi.org/10.1084/jem.20132183
_version_ 1782479921282547712
author Stock, Angus T.
Smith, Jeffrey M.
Carbone, Francis R.
author_facet Stock, Angus T.
Smith, Jeffrey M.
Carbone, Francis R.
author_sort Stock, Angus T.
collection PubMed
description Infection induces the expression of inflammatory chemokines that recruit immune cells to the site of inflammation. Whereas tissues such as the intestine and skin express unique chemokines during homeostasis, whether different tissues express distinct chemokine profiles during inflammation remains unclear. With this in mind, we performed a comprehensive screen of the chemokines expressed by two tissues (skin and sensory ganglia) infected with a common viral pathogen (herpes simplex virus type 1). After infection, the skin and ganglia showed marked differences in their expression of the family of Cxcr2 chemokine ligands. Specifically, Cxcl1/2/3, which in turn controlled neutrophil recruitment, was up-regulated in the skin but absent from the ganglia. Within the ganglia, Cxcl2 expression and subsequent neutrophil recruitment was inhibited by type I interferon (IFN). Using a combination of bone marrow chimeras and intracellular chemokine staining, we show that type I IFN acted by directly suppressing Cxcl2 expression by monocytes, abrogating their ability to recruit neutrophils to the ganglia. Overall, our findings describe a novel role for IFN in the direct, and selective, inhibition of Cxcr2 chemokine ligands, which results in the inhibition of neutrophil recruitment to neuronal tissue.
format Online
Article
Text
id pubmed-4010892
institution National Center for Biotechnology Information
language English
publishDate 2014
publisher The Rockefeller University Press
record_format MEDLINE/PubMed
spelling pubmed-40108922014-11-05 Type I IFN suppresses Cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection Stock, Angus T. Smith, Jeffrey M. Carbone, Francis R. J Exp Med Brief Definitive Report Infection induces the expression of inflammatory chemokines that recruit immune cells to the site of inflammation. Whereas tissues such as the intestine and skin express unique chemokines during homeostasis, whether different tissues express distinct chemokine profiles during inflammation remains unclear. With this in mind, we performed a comprehensive screen of the chemokines expressed by two tissues (skin and sensory ganglia) infected with a common viral pathogen (herpes simplex virus type 1). After infection, the skin and ganglia showed marked differences in their expression of the family of Cxcr2 chemokine ligands. Specifically, Cxcl1/2/3, which in turn controlled neutrophil recruitment, was up-regulated in the skin but absent from the ganglia. Within the ganglia, Cxcl2 expression and subsequent neutrophil recruitment was inhibited by type I interferon (IFN). Using a combination of bone marrow chimeras and intracellular chemokine staining, we show that type I IFN acted by directly suppressing Cxcl2 expression by monocytes, abrogating their ability to recruit neutrophils to the ganglia. Overall, our findings describe a novel role for IFN in the direct, and selective, inhibition of Cxcr2 chemokine ligands, which results in the inhibition of neutrophil recruitment to neuronal tissue. The Rockefeller University Press 2014-05-05 /pmc/articles/PMC4010892/ /pubmed/24752295 http://dx.doi.org/10.1084/jem.20132183 Text en © 2014 Stock et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Brief Definitive Report
Stock, Angus T.
Smith, Jeffrey M.
Carbone, Francis R.
Type I IFN suppresses Cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection
title Type I IFN suppresses Cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection
title_full Type I IFN suppresses Cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection
title_fullStr Type I IFN suppresses Cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection
title_full_unstemmed Type I IFN suppresses Cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection
title_short Type I IFN suppresses Cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection
title_sort type i ifn suppresses cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection
topic Brief Definitive Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4010892/
https://www.ncbi.nlm.nih.gov/pubmed/24752295
http://dx.doi.org/10.1084/jem.20132183
work_keys_str_mv AT stockangust typeiifnsuppressescxcr2drivenneutrophilrecruitmentintothesensorygangliaduringviralinfection
AT smithjeffreym typeiifnsuppressescxcr2drivenneutrophilrecruitmentintothesensorygangliaduringviralinfection
AT carbonefrancisr typeiifnsuppressescxcr2drivenneutrophilrecruitmentintothesensorygangliaduringviralinfection