Ryo Hayakari, 1 Tomoh Matsumiya, 1,* Fei Xing, 1 Janeth C. Tayone, 1 Junichi Dempoya, 2 Tetsuya Tatsuta, 3 Tomomi Aizawa-Yashiro, 4 Tadaatsu Imaizumi, 1 Hidemi Yoshida 1 and Kei Satoh. 1
Institutions
1 Department of Vascular Biology, Institute of Brain Science, 2 Department of Cardiology, Respiratory Medicine and Nephrology, 3 Department of Gastroenterology and Hematology, and 4 Department of Pediatrics, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Abstract
BACKGROUND: Propolis is a bee product with various biological properties, including an antiviral activity when taken orally. However, its mechanisms at the cellular and molecular level are not well understood.
RESULTS:
We investigated the effect of propolis on antiviral signaling in A549 cells transfected with double-stranded RNA (dsRNA), a model for viral infection. Pretreatment of the cells with propolis inhibited poly I:C (synthetic dsRNA)-induced interferon (IFN)-β expression. Propolis had no effect on the dsRNA-induced expression of RIG-I-like receptors (RLRs), which are known as intracellular viral RNA sensors. As to the effect on antiviral executor genes, propolis enhanced myxovirus resistance 1 (MX1) expression, whereas interferon-inducible gene 6-16 (G1P3) and 2′-5′-oligoadenylate synthetase (OAS) were unaffected. All of these genes belong to the IFN-inducible genes, suggesting that the effect of propolis on antiviral signaling is not necessarily mediated by the autocrine regulation by IFN-β. Propolis pretreatment inhibited dsRNA-induced interleukin-8 (IL8) and CCL5 expression, and consequently lowered polymorphonuclear leukocyte (PMN) chemotactic activity in the cell-conditioned medium.
CONCLUSION:
Taken together, these results suggest that propolis may suppress excess inflammatory responses without affecting the innate immunity during viral infection.
* THESE STATEMENTS HAVE NOT BEEN EVALUATED BY THE FOOD AND DRUG ADMINISTRATION. THIS IS NOT INTENDED TO DIAGNOSE, TREAT CURE OR PREVENT ANY DISEASE.