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Viral inhibition of bacterial phagocytosis by human macrophages: redundant role of CD36

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.
1932-6203
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
1a5f95d6-c7a5-4787-89be-269d1c1e863a
Wallington, Joshua
7f2909e0-96f1-4237-b2c2-ea3aa695a9d1
Bastidas Legarda, Leidy Y.
66bd5603-1c85-4321-a129-20ced5b35e4c
Nicholas, Benjamin
785c44fb-6536-4189-803b-4545425e9385
Chidomere, Chiamaka
abdd302d-47ba-4851-ac27-47541c95f3d5
Robinson, Emily C.
747299fc-f38e-4423-8b50-9e7aed710ea4
Martin, Kirstin
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Tocheva, Anna S.
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Christodoulides, Myron
eba99148-620c-452a-a334-c1a52ba94078
Djukanovic, Ratko
d9a45ee7-6a80-4d84-a0ed-10962660a98d
Wilkinson, Thomas M.A.
8c55ebbb-e547-445c-95a1-c8bed02dd652
Staples, Karl J
e0e9d80f-0aed-435f-bd75-0c8818491fee

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), 1-15. (doi:10.1371/journal.pone.0163889). (PMID:27701435)

Record type: Article

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

Identifiers

Local EPrints ID: 401150
URI: https://eprints.soton.ac.uk/id/eprint/401150
ISSN: 1932-6203
PURE UUID: 1f0e501c-8882-480a-ab36-5283d1de97c4
ORCID for Ratko Djukanovic: ORCID iD orcid.org/0000-0001-6039-5612
ORCID for Karl J Staples: ORCID iD orcid.org/0000-0003-3844-6457

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Date deposited: 10 Oct 2016 11:25
Last modified: 03 Dec 2019 02:07

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Contributors

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
Author: Karl J Staples ORCID iD

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