AI Article Synopsis
- The NF-κB pathway is crucial for immune responses, cell growth, inflammation, and tumor development.
- During HSV-1 viral replication, the NF-κB pathway is activated in monocytic cells, with the phosphorylation of the p65 protein linked to active virus replication.
- The expression of miR-146a during this process requires NF-κB activation and plays a role in regulating IRAK1, as shown by the lack of miR-146a upregulation in THP-1 DN IκBα cells infected with HSV-1.
Article Abstract
The nuclear factor κB (NF-κB) pathway plays a key role in innate and adaptive immunity, cell proliferation and survival, inflammation and tumors development. MiR-146a is an immune system regulator that has anti-inflammatory function in multiple cell types and conditions. Here we demonstrate activation of canonical NF-κB pathway in monocytic cells upon HSV-1 replication. By constructing and using a recombinant HSV-1\EGFP virus, we monitored the capability of the virus to recruit NF-κB and we report that the phosphorylation of p65 protein correlates with an active virus replication at single-cell level. In addition, we found that upregulation of miR-146a during viral replication is strictly dependent on NF-κB activation and correlates with tight control of the interleukin-1 receptor-associate kinase 1 (IRAK1). Accordingly, THP-1 DN IκBα cells, expressing a dominant negative mIκBα, did not show upregulation of miR-146a upon HSV-1 infection. Our data suggest that the expression of miRNA-146a modulates NF-κB activation through targeting IRAK1 during HSV-1 replication in THP-1 cells.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6435682 | PMC |
| http://dx.doi.org/10.1038/s41598-019-41530-5 | DOI Listing |
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