Article

Hovenia monofloral honey can attenuate Enterococcus faecalis mediated biofilm formation and inflammation

Ri You1, Oh Yun Kwon1, Hyun Joo Woo1, Seung Ho Lee1,*
Author Information & Copyright
1Department of Nano-Bioengineering, Incheon National University, Incheon 22122, Korea.
*Corresponding Author: Seung Ho Lee, Department of Nano-Bioengineering, Incheon National University, Incheon 22122, Korea. E-mail: lsh1602@gmail.com.

© Copyright 2021 Korean Society for Food Science of Animal Resources. This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Received: Oct 18, 2021 ; Revised: Nov 16, 2021 ; Accepted: Nov 16, 2021

Published Online: Nov 26, 2021

Abstract

We evaluated the anti-biofilm formation and anti-inflammatory activity of Hovenia monofloral honey (HMH) against Enterococcus faecalis. Co-culture of HMH with E. faecalis attenuated the biofilm formation of E. faecalis on a polystyrene surface. In addition, HMH effectively eradicated the established E. faecalis biofilm. HMH significantly attenuated E. faecalis growth but did not affect the production of extracellular polymeric substances (EPSs) on E. faecalis, indicating that reduction of E. faecalis biofilm is a result of HMH-mediated killing of E. faecalis. Furthermore, we found that HMH can effectively attenuate E. faecalis-induced expression of a proinflammatory interleukin-8 (IL-8) in HT-29 cells. Interestingly, treatment of HMH significantly attenuated the E. faecalis-mediated expression of Toll-like receptor-2 (TLR-2) and its adaptor molecules, myeloid differentiation primary response 88 (MyD88), in HT-29 cells. In addition, E. faecalis-induced mitogen-activated protein kinases (MAPKs) phosphorylation was significantly attenuated by HMH administration. Furthermore, HMH-mediated anti-inflammatory efficacy (0.2 mg/mL of HMHs) had an equal extent of inhibitory efficacy as 5 µM of MyD88 inhibitor to attenuate E. faecalis-mediated IL-8 expression in HT-29 cells. These results suggest that HMH could effectively inhibit E. faecalis-mediated gastrointestinal inflammation through regulating the TLR-2/MyD88/MAPKs signaling pathways. Collectively, our data suggest that HMH could be developed as a potential natural agent to control E. faecalis-mediated biofilm formation and inflammation.

Keywords: Honvenia monofloral honey; Enterococcus faecalis; biofilm; inflammation; Toll like receptor-2; MAPKs