Journal
JOURNAL OF INNATE IMMUNITY
Volume 8, Issue 5, Pages 452-463Publisher
KARGER
DOI: 10.1159/000446824
Keywords
Macrophages; Type I interferons; Pattern recognition receptors
Categories
Funding
- Career Development Award from the Medical Research Council [G0800311]
- MRC [G1001763]
- Marie Curie Career Integration Grant from the European Commission
- National Heart and Lung Institute Foundation [1048073]
- Rosetrees Trust [M370]
- Wellcome Trust [104931/Z/14/Z]
- BBSRC [BB/L015129/1]
- Biotechnology and Biological Sciences Research Council [BB/L015129/1] Funding Source: researchfish
- Medical Research Council [G1001763, G0800311] Funding Source: researchfish
- MRC [G0800311] Funding Source: UKRI
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Respiratory syncytial virus (RSV) is a common cause of lower respiratory tract infections. Immunity to RSV is initiated upon detection of the virus by pattern recognition receptors, such as RIG-I-like receptors. RIG-I-like receptors signal via MAVS to induce the synthesis of proinflammatory mediators, including type I interferons (IFNs), which trigger and shape antiviral responses and protect cells from infection. Alveolar macrophages (AMs) are amongst the first cells to encounter invading viruses and the ones producing type I IFNs. However, it is unclear whether IFNs act to prevent AMs from serving as vehicles for viral replication. In this study, primary AMs from MAVS (Mays(-/-))- or type I IFN receptor (Ifnar1(-/-))-deficient mice were exposed to RSV ex vivo. Wild-type (wt) AMs but not Mavs(-/-) and Ifnar1(-/-) AMs produced inflammatory mediators in response to RSV. Furthermore, Mays and Ifnar1(-/-) AMs accumulated more RSV proteins than wt AMs, but the infection was abortive. Thus, RIG-I-like receptor-MAVS and IFNAR signalling are important for the induction of proinflammatory mediators from AMs upon RSV infection, but this signalling is not central for controlling viral replication. The ability to restrict viral replication makes AMs ideal sensors of RSV infection and important initiators of immune responses in the lung. (C) 2016 The Author(s) Published by S. Karger AG, Basel
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