Influenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.

Influenza virus infection accounts for significant morbidity and mortality world-wide. Interactions of the virus with host cells, particularly those of the macrophage lineage, are thought to contribute to various pathological changes associated with poor patient outcome. Development of new strategie...

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Autores principales:	Marieke A Hoeve, Anthony A Nash, David Jackson, Richard E Randall, Ian Dransfield
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/d7bcc96508bd45e9b366562108e30912
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spelling	oai:doaj.org-article:d7bcc96508bd45e9b366562108e309122021-11-18T07:30:58ZInfluenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.1932-620310.1371/journal.pone.0029443https://doaj.org/article/d7bcc96508bd45e9b366562108e309122012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22238612/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Influenza virus infection accounts for significant morbidity and mortality world-wide. Interactions of the virus with host cells, particularly those of the macrophage lineage, are thought to contribute to various pathological changes associated with poor patient outcome. Development of new strategies to treat disease therefore requires a detailed understanding of the impact of virus infection upon cellular responses. Here we report that human blood-derived monocytes could be readily infected with the H3N2 influenza virus A/Udorn/72 (Udorn), irrespective of their phenotype (CD14(++)/CD16(-), CD14(++)/CD16(+) or CD14(dim)CD16(++)), as determined by multi-colour flow cytometry for viral haemagglutinin (HA) expression and cell surface markers 8-16 hours post infection. Monocytes are relatively resistant to influenza-induced cell death early in infection, as approximately 20% of cells showed influenza-induced caspase-dependent apoptosis. Infection of monocytes with Udorn also induced the release of IL-6, IL-8, TNFα and IP-10, suggesting that NS1 protein of Udorn does not (effectively) inhibit this host defence response in human monocytes. Comparative analysis of human monocyte-derived macrophages (Mph) demonstrated greater susceptibility to human influenza virus than monocytes, with the majority of both pro-inflammatory Mph1 and anti-inflammatory/regulatory Mph2 cells expressing viral HA after infection with Udorn. Influenza infection of macrophages also induced cytokine and chemokine production. However, both Mph1 and Mph2 phenotypes released comparable amounts of TNFα, IL-12p40 and IP-10 after infection with H3N2, in marked contrast to differential responses to LPS-stimulation. In addition, we found that influenza virus infection augmented the capacity of poorly phagocytic Mph1 cells to phagocytose apoptotic cells by a mechanism that was independent of either IL-10 or the Mer receptor tyrosine kinase/Protein S pathway. In summary, our data reveal that influenza virus infection of human macrophages causes functional alterations that may impact on the process of resolution of inflammation, with implications for viral clearance and lung pathology.Marieke A HoeveAnthony A NashDavid JacksonRichard E RandallIan DransfieldPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 1, p e29443 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Marieke A Hoeve Anthony A Nash David Jackson Richard E Randall Ian Dransfield Influenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.
description	Influenza virus infection accounts for significant morbidity and mortality world-wide. Interactions of the virus with host cells, particularly those of the macrophage lineage, are thought to contribute to various pathological changes associated with poor patient outcome. Development of new strategies to treat disease therefore requires a detailed understanding of the impact of virus infection upon cellular responses. Here we report that human blood-derived monocytes could be readily infected with the H3N2 influenza virus A/Udorn/72 (Udorn), irrespective of their phenotype (CD14(++)/CD16(-), CD14(++)/CD16(+) or CD14(dim)CD16(++)), as determined by multi-colour flow cytometry for viral haemagglutinin (HA) expression and cell surface markers 8-16 hours post infection. Monocytes are relatively resistant to influenza-induced cell death early in infection, as approximately 20% of cells showed influenza-induced caspase-dependent apoptosis. Infection of monocytes with Udorn also induced the release of IL-6, IL-8, TNFα and IP-10, suggesting that NS1 protein of Udorn does not (effectively) inhibit this host defence response in human monocytes. Comparative analysis of human monocyte-derived macrophages (Mph) demonstrated greater susceptibility to human influenza virus than monocytes, with the majority of both pro-inflammatory Mph1 and anti-inflammatory/regulatory Mph2 cells expressing viral HA after infection with Udorn. Influenza infection of macrophages also induced cytokine and chemokine production. However, both Mph1 and Mph2 phenotypes released comparable amounts of TNFα, IL-12p40 and IP-10 after infection with H3N2, in marked contrast to differential responses to LPS-stimulation. In addition, we found that influenza virus infection augmented the capacity of poorly phagocytic Mph1 cells to phagocytose apoptotic cells by a mechanism that was independent of either IL-10 or the Mer receptor tyrosine kinase/Protein S pathway. In summary, our data reveal that influenza virus infection of human macrophages causes functional alterations that may impact on the process of resolution of inflammation, with implications for viral clearance and lung pathology.
format	article
author	Marieke A Hoeve Anthony A Nash David Jackson Richard E Randall Ian Dransfield
author_facet	Marieke A Hoeve Anthony A Nash David Jackson Richard E Randall Ian Dransfield
author_sort	Marieke A Hoeve
title	Influenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.
title_short	Influenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.
title_full	Influenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.
title_fullStr	Influenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.
title_full_unstemmed	Influenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.
title_sort	influenza virus a infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/d7bcc96508bd45e9b366562108e30912
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Influenza virus A infection of human monocyte and macrophage subpopulations reveals increased susceptibility associated with cell differentiation.

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