期刊
VIROLOGY
卷 526, 期 -, 页码 155-164出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2018.10.017
关键词
Influenza A virus; Lung inflammation; IFN gamma; Host response
类别
资金
- Biotechnology and Biological Sciences Research Council Institute Strategic Program [BB/J004324/1, BB/P013740/1]
- Scottish Higher Education Fund Council grant
- ICHAIR-BBSRC Studentship
- BBSRC [BBS/E/D/20241864, BBS/E/D/20002174, BBS/E/D/20002173] Funding Source: UKRI
IFN gamma is a key regulator of inflammatory responses but its role in influenza A virus (IAV) pathogenesis is unclear. Our studies show that infection of mice lacking the IFN gamma receptor (IFN gamma R-/-) at a dose which caused severe disease in wild type 129 Sv/Ev (WT) mice resulted in milder clinical symptoms and significantly lower lung virus titers by 6 days post-infection (dpi). Viral spread was reduced in IFN gamma R-/- lungs at 2 and 4 dpi. Levels of inflammatory cytokines and chemokines were lower in IFN gamma R-/- mice at 2 dpi and there was less infiltration of monocyte/macrophage lineage cells than in WT mice. There was no difference in CD4(+) and CD8(+) T cells and alveolar macrophages in the bronchoalveolar lavage fluid (BALF) at 2 and 4 dpi but by 4 dpi IFN gamma R-/- mice had significantly higher percentages of neutrophils. Our data strongly suggest that IAV can use the inflammatory response to promote viral spread.
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