期刊
PLOS PATHOGENS
卷 6, 期 11, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1001178
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资金
- British Lung Foundation (BLF) [P06/3]
- Medical Research Council (MRC) [G0601236]
- Asthma UK [RF07/04, 02/027, 05/067]
- Medical Research Council
- British Medical Association
- British Lung Foundation/Severin Wunderman Family Foundation [P00/2]
- Wellcome Trust [083567/Z/07/Z]
- National Institute for Health Research Biomedical Research Centre
- Imperial College
- Asthma UK [05/067, RF07/04] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BB/E52708X/1] Funding Source: researchfish
- Medical Research Council [G0700552, G0601236] Funding Source: researchfish
- BBSRC [BB/E52708X/1] Funding Source: UKRI
- MRC [G0700552, G0601236] Funding Source: UKRI
The relative roles of the endosomal TLR3/7/8 versus the intracellular RNA helicases RIG-I and MDA5 in viral infection is much debated. We investigated the roles of each pattern recognition receptor in rhinovirus infection using primary bronchial epithelial cells. TLR3 was constitutively expressed; however, RIG-I and MDA5 were inducible by 8-12 h following rhinovirus infection. Bronchial epithelial tissue from normal volunteers challenged with rhinovirus in vivo exhibited low levels of RIG-I and MDA5 that were increased at day 4 post infection. Inhibition of TLR3, RIG-I and MDA5 by siRNA reduced innate cytokine mRNA, and increased rhinovirus replication. Inhibition of TLR3 and TRIF using siRNA reduced rhinovirus induced RNA helicases. Furthermore, IFNAR1 deficient mice exhibited RIG-I and MDA5 induction early during RV1B infection in an interferon independent manner. Hence anti-viral defense within bronchial epithelium requires co-ordinated recognition of rhinovirus infection, initially via TLR3/TRIF and later via inducible RNA helicases.
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