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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 J+Gen+Virol
2015 ; 96
(10
): 2951-2960
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Susceptibility of bone marrow-derived macrophages to influenza virus infection is
dependent on macrophage phenotype
#MMPMID26297234
Campbell GM
; Nicol MQ
; Dransfield I
; Shaw DJ
; Nash AA
; Dutia BM
J Gen Virol
2015[Oct]; 96
(10
): 2951-2960
PMID26297234
show ga
The role of the macrophage in influenza virus infection is complex. Macrophages
are critical for resolution of influenza virus infections but implicated in
morbidity and mortality in severe infections. They can be infected with influenza
virus and consequently macrophage infection is likely to have an impact on the
host immune response. Macrophages display a range of functional phenotypes, from
the prototypical pro-inflammatory classically activated cell to alternatively
activated anti-inflammatory macrophages involved in immune regulation and wound
healing. We were interested in how macrophages of different phenotype respond to
influenza virus infection and therefore studied the infection of bone
marrow-derived macrophages (BMDMs) of classical and alternative phenotype in
vitro. Our results show that alternatively activated macrophages are more readily
infected and killed by the virus than classically activated. Classically
activated BMDMs express the pro-inflammatory markers inducible nitric oxide
synthase (iNOS) and TNF-?, and TNF-? expression was further upregulated following
infection. Alternatively activated macrophages express Arginase-1 and CD206;
however, following infection, expression of these markers was downregulated
whilst expression of iNOS and TNF-? was upregulated. Thus, infection can override
the anti-inflammatory state of alternatively activated macrophages. Importantly,
however, this results in lower levels of pro-inflammatory markers than those
produced by classically activated cells. Our results showed that macrophage
phenotype affects the inflammatory macrophage response following infection, and
indicated that modulating the macrophage phenotype may provide a route to develop
novel strategies to prevent and treat influenza virus infection.