PMID- 26297234
OWN - NLM
STAT- MEDLINE
DCOM- 20160119
LR  - 20210103
IS  - 1465-2099 (Electronic)
IS  - 0022-1317 (Print)
IS  - 0022-1317 (Linking)
VI  - 96
IP  - 10
DP  - 2015 Oct
TI  - Susceptibility of bone marrow-derived macrophages to influenza virus infection is 
      dependent on macrophage phenotype.
PG  - 2951-2960
LID - 10.1099/jgv.0.000240 [doi]
AB  - 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-alpha, and TNF-alpha 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-alpha 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.
FAU - Campbell, Gillian M
AU  - Campbell GM
AD  - The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of 
      Edinburgh, Edinburgh EH25 9RG, UK.
FAU - Nicol, Marlynne Q
AU  - Nicol MQ
AD  - The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of 
      Edinburgh, Edinburgh EH25 9RG, UK.
FAU - Dransfield, Ian
AU  - Dransfield I
AD  - Centre for Inflammation Research, Queen's Medical Research Institute, University 
      of Edinburgh, Edinburgh EH16 4TL, UK.
FAU - Shaw, Darren J
AU  - Shaw DJ
AD  - The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of 
      Edinburgh, Edinburgh EH25 9RG, UK.
FAU - Nash, Anthony A
AU  - Nash AA
AD  - The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of 
      Edinburgh, Edinburgh EH25 9RG, UK.
FAU - Dutia, Bernadette M
AU  - Dutia BM
AD  - The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of 
      Edinburgh, Edinburgh EH25 9RG, UK.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150709
PL  - England
TA  - J Gen Virol
JT  - The Journal of general virology
JID - 0077340
SB  - IM
MH  - Animals
MH  - Cell Survival
MH  - Cells, Cultured
MH  - Female
MH  - *Host-Pathogen Interactions
MH  - Immunophenotyping
MH  - Influenza A virus/*growth & development
MH  - Macrophages/immunology/*physiology/*virology
MH  - Mice, 129 Strain
MH  - *Phenotype
PMC - PMC4635478
EDAT- 2015/08/25 06:00
MHDA- 2016/01/20 06:00
PMCR- 2015/10/01
CRDT- 2015/08/23 06:00
PHST- 2015/08/23 06:00 [entrez]
PHST- 2015/08/25 06:00 [pubmed]
PHST- 2016/01/20 06:00 [medline]
PHST- 2015/10/01 00:00 [pmc-release]
AID - 000240 [pii]
AID - 10.1099/jgv.0.000240 [doi]
PST - ppublish
SO  - J Gen Virol. 2015 Oct;96(10):2951-2960. doi: 10.1099/jgv.0.000240. Epub 2015 Jul 
      9.