Abstract
Pharyngitis is an inflammation of the pharynx caused by viral, bacterial, or non-infectious factors. In the present study, the anti-inflammatory efficacy of carvacrol was assessed using an in vitro model of streptococcal pharyngitis using human tonsil epithelial cells (HTonEpiCs) induced with Streptococcus pyogenes cell wall antigens. HTonEpiCs were stimulated by a mixture of lipoteichoic acid (LTA) and peptidoglycan (PGN) for 4 h followed by exposure to carvacrol for 20 h. Following exposure, interleukin (IL)-6, IL-8, human beta defensin-2 (HBD-2), epithelial-derived neutrophil-activating protein-78 (ENA-78), granulocyte chemotactic protein-2 (GCP-2), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-α), and prostaglandin (PGE2) were measured by enzyme-linked immunosorbent assays (ELISA). The levels of pro-inflammatory cytokines, IL-6, IL-8, ENA-78, and GCP-2 were decreased in a carvacrol dose-dependent manner. The production of HBD-2 was significantly suppressed over 24 h carvacrol treatments. PGE2 and COX-2 levels in the cell suspensions were affected by carvacrol treatment. TNF-α was not detected. The cell viability of all the tested carvacrol concentrations was greater than 80%, with no morphological changes. The results suggest that carvacrol has anti-inflammatory properties, and carvacrol needs to be further assessed for potential clinical or healthcare applications to manage the pain associated with streptococcal pharyngitis.
Highlights
Inflammation is a natural defense mechanism of the body designed to eliminate harmful stimuli, including exogenous pathogens, and initiate the healing process through various chemical mediators and signaling pathways [1]
To further assess whether carvacrol has a harmful effect on HTonEpiCs, the cells were incubated with carvacrol (8–250 μg/mL) or controls (DMSO as vehicle control, nimesulide as positive control) and the cell viability was analyzed by flow cytometry
The results showed that carvacrol at the tested concentrations was not cytotoxic (>80% cell viability) to HTonEpiCs by flow cytometric cell viability assay (Figure 3A,B)
Summary
Inflammation is a natural defense mechanism of the body designed to eliminate harmful stimuli, including exogenous pathogens, and initiate the healing process through various chemical mediators and signaling pathways [1]. The tonsillar epithelial cells recognize S. pyogenes cell wall antigens through Toll-like receptors (TLR), such as TLR-2 These receptors identify pathogen-associated molecular patterns, including lipoteichoic acid (LTA) and peptidoglycan (PGN) [5,6]. We have previously shown that the ethanol and aqueous extracts of several herbal plants possess anti-inflammatory activities, decreasing the production of tonsil cell-associated inflammatory mediators, including cytokines, such as interleukin (IL)-8, human beta defensin-2 (HBD-2), granulocyte chemotactic protein-2 (GCP-2), and epithelial-derived neutrophil-activating protein-78 (ENA-78) [9]. The effect of carvacrol on S. pyogenes antigen-induced tonsil epithelial cells and its inflammatory mediator production has not been reported. The present study investigated the impact of carvacrol on cytokine production by the tonsil epithelial cells (HTonEpiCs) following LTA and PGN stimulation
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
