Viral inhibition of bacterial phagocytosis by human macrophages: redundant role of CD36
Viral inhibition of bacterial phagocytosis by human macrophages: redundant role of CD36
Macrophages are essential to maintaining lung homoeostasis and recent work has demonstrated that influenza-infected lung macrophages downregulate their expression of the scavenger receptor CD36. This receptor has also been shown to be involved in phagocytosis of Streptococcus pneumoniae, a primary agent associated with pneumonia secondary to viral infection. The aim of this study was to investigate the role of CD36 in the effects of viral infection on macrophage phagocytic function. Human monocyte-derived macrophages (MDM) were exposed to H3N2 X31 influenza virus, M37 respiratory syncytial virus (RSV) or UV-irradiated virus. No infection of MDM was seen upon exposure to UV-irradiated virus but incubation with live X31 or M37 resulted in significant levels of viral detection by flow cytometry or RT-PCR respectively. Infection resulted in significantly diminished uptake of S. pneumoniae by MDM and significantly decreased expression of CD36 at both the cell surface and mRNA level. Concurrently, there was a significant increase in IFN? gene expression in response to infection and we observed a significant decrease in bacterial phagocytosis (p = 0.031) and CD36 gene expression (p = 0.031) by MDM cultured for 24 h in 50IU/ml IFN?. Knockdown of CD36 by siRNA resulted in decreased phagocytosis, but this was mimicked by transfection reagent alone. When MDM were incubated with CD36 blocking antibodies no effect on phagocytic ability was observed. These data indicate that autologous IFN? production by virally-infected cells can inhibit bacterial phagocytosis, but that decreased CD36 expression by these cells does not play a major role in this functional deficiency.
1-15
Cooper, Grace E
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Pounce, Zoe C
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Wallington, Joshua
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Bastidas Legarda, Leidy Y.
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Nicholas, Benjamin
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Chidomere, Chiamaka
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Robinson, Emily C.
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Martin, Kirstin
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Tocheva, Anna S.
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Christodoulides, Myron
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Djukanovic, Ratko
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Wilkinson, Thomas M.A.
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Staples, Karl J
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Cooper, Grace E
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Pounce, Zoe C
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Wallington, Joshua
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Bastidas Legarda, Leidy Y.
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Nicholas, Benjamin
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Chidomere, Chiamaka
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Robinson, Emily C.
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Martin, Kirstin
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Tocheva, Anna S.
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Christodoulides, Myron
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Djukanovic, Ratko
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Wilkinson, Thomas M.A.
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Staples, Karl J
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Cooper, Grace E, Pounce, Zoe C, Wallington, Joshua, Bastidas Legarda, Leidy Y., Nicholas, Benjamin, Chidomere, Chiamaka, Robinson, Emily C., Martin, Kirstin, Tocheva, Anna S., Christodoulides, Myron, Djukanovic, Ratko, Wilkinson, Thomas M.A. and Staples, Karl J
(2016)
Viral inhibition of bacterial phagocytosis by human macrophages: redundant role of CD36.
PLoS ONE, 11 (10), .
(doi:10.1371/journal.pone.0163889).
(PMID:27701435)
Abstract
Macrophages are essential to maintaining lung homoeostasis and recent work has demonstrated that influenza-infected lung macrophages downregulate their expression of the scavenger receptor CD36. This receptor has also been shown to be involved in phagocytosis of Streptococcus pneumoniae, a primary agent associated with pneumonia secondary to viral infection. The aim of this study was to investigate the role of CD36 in the effects of viral infection on macrophage phagocytic function. Human monocyte-derived macrophages (MDM) were exposed to H3N2 X31 influenza virus, M37 respiratory syncytial virus (RSV) or UV-irradiated virus. No infection of MDM was seen upon exposure to UV-irradiated virus but incubation with live X31 or M37 resulted in significant levels of viral detection by flow cytometry or RT-PCR respectively. Infection resulted in significantly diminished uptake of S. pneumoniae by MDM and significantly decreased expression of CD36 at both the cell surface and mRNA level. Concurrently, there was a significant increase in IFN? gene expression in response to infection and we observed a significant decrease in bacterial phagocytosis (p = 0.031) and CD36 gene expression (p = 0.031) by MDM cultured for 24 h in 50IU/ml IFN?. Knockdown of CD36 by siRNA resulted in decreased phagocytosis, but this was mimicked by transfection reagent alone. When MDM were incubated with CD36 blocking antibodies no effect on phagocytic ability was observed. These data indicate that autologous IFN? production by virally-infected cells can inhibit bacterial phagocytosis, but that decreased CD36 expression by these cells does not play a major role in this functional deficiency.
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Accepted/In Press date: 18 September 2016
e-pub ahead of print date: 4 October 2016
Organisations:
Clinical & Experimental Sciences
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Local EPrints ID: 401150
URI: http://eprints.soton.ac.uk/id/eprint/401150
ISSN: 1932-6203
PURE UUID: 1f0e501c-8882-480a-ab36-5283d1de97c4
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Date deposited: 10 Oct 2016 11:25
Last modified: 16 Mar 2024 02:38
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Author:
Grace E Cooper
Author:
Zoe C Pounce
Author:
Joshua Wallington
Author:
Leidy Y. Bastidas Legarda
Author:
Benjamin Nicholas
Author:
Chiamaka Chidomere
Author:
Emily C. Robinson
Author:
Kirstin Martin
Author:
Anna S. Tocheva
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