Toll-like receptor 4 siRNA attenuates LPS-induced secretion of inflammatory cytokines and chemokines by macrophages
Journal of Infection, ISSN: 0163-4453, Vol: 55, Issue: 1, Page: e1-e9
2007
- 29Citations
- 24Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations29
- Citation Indexes29
- 29
- CrossRef21
- Captures24
- Readers24
- 24
Article Description
Toll-like receptor 4 (TLR4) is critical for activation of macrophages by Lipopolysaccharide (LPS). In this study, we investigated the silencing effects of TLR4-specific 21-nt small interfering RNAs (siRNA) on TLR4 expression in RAW264.7 cells. It was found that treatment with TLR4 siRNA down-regulated the TLR4 mRNA and protein expression in macrophage RAW264.7 cells, and reduced the sensitivity of the cells to LPS stimulation. Our findings also demonstrate that treatment with TLR4 siRNA significantly decreased the tumor necrosis factor-α (TNF-α) and macrophage inflammatory protein 2 (MIP-2) expression induced by LPS. TLR4 siRNA treatment also impaired the signalling of mitogen-activated protein kinases (MAPK) induced by LPS in RAW264.7 cells. These data suggest that inhibition of TLR4 expression by TLR4 siRNA may be therapeutically beneficial in controlling the overall responses of immune cells to LPS.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0163445307000138; http://dx.doi.org/10.1016/j.jinf.2007.01.003; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=34249997787&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/17336389; https://linkinghub.elsevier.com/retrieve/pii/S0163445307000138; https://dx.doi.org/10.1016/j.jinf.2007.01.003
Elsevier BV
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