Journal
BIOMEDICINES
Volume 10, Issue 2, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines10020492
Keywords
host defense peptide; innate immunity; NF-kappa B; poly L:C; toll-like receptor 3
Categories
Funding
- Alfred Osterlund Foundation
- Royal Physiographic Society
- Research Funds for Oral Health Related Research by Region Skane [732821]
- Swedish Heart and Lung Foundation [20180207]
- Swedish Medical Research Council [2020-00922]
- Swedish Research Council [2020-00922] Funding Source: Swedish Research Council
- Swedish Heart-Lung Foundation [20180207] Funding Source: Swedish Heart-Lung Foundation
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LL-37 enhances poly I:C-induced expression of TLR3 mRNA and protein, possibly through enhanced import of poly I:C. Dexamethasone reduces LL-37/poly I:C-induced TLR3 expression by attenuating NF-kappa B activity.
The human host defense peptide LL-37 influences double-stranded RNA signaling, but this process is not well understood. Here, we investigate synergistic actions of LL-37 and synthetic double-stranded RNA (poly I:C) on toll-like receptor 3 (TLR3) expression and signaling, and examine underlying mechanisms. In bronchial epithelial BEAS-2B cells, LL-37 potentiated poly I:C-induced TLR3 mRNA and protein expression demonstrated by qPCR and Western blot, respectively. Interestingly, these effects were associated with increased uptake of rhodamine-tagged poly I:C visualized by immunocytochemistry. The LL-37/poly I:C-induced upregulation of TLR3 mRNA expression was prevented by the endosomal acidification inhibitor chloroquine, indicating involvement of downstream TLR3 signaling. The glucocorticoid dexamethasone reduced LL-37/poly I:C-induced TLR3 expression on both mRNA and protein levels, and this effect was associated with increased I kappa B alpha protein expression, suggesting that dexamethasone acts via attenuation of NF-kappa B activity. We conclude that LL-37 potentiates poly I:C-induced upregulation of TLR3 through a mechanism that may involve enhanced import of poly I:C and that LL-37/poly I:C-induced TLR3 expression is associated with downstream TLR3 signaling and sensitive to inhibition of NF-kappa B activity.
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