Context: Clove (Eugenia caryophyllata Thunb. [Myrtaceae]) essential oil (CEO) has been shown to possess antimicrobial, antifungal, antiviral, antioxidant, anti-inflammatory and anticancer properties. However, few studies have focused on its topical use.Objective: We investigated the biological activity of a commercially available CEO in a human skin disease model.Materials and methods: We evaluated the effect of CEO on 17 protein biomarkers that play critical roles in inflammation and tissue remodelling in a validated human dermal fibroblast system, which was designed to model chronic inflammation and fibrosis. Four concentrations of CEO (0.011, 0.0037, 0.0012, and 0.00041%, v/v) were studied. The effect of 0.011% CEO on genome-wide gene expression was also evaluated.Results and discussion: CEO at a concentration of 0.011% showed robust antiproliferative effects on human dermal fibroblasts. It significantly inhibited the increased production of several proinflammatory biomarkers such as vascular cell adhesion molecule-1 (VCAM-1), interferon γ-induced protein 10 (IP-10), interferon-inducible T-cell α chemoattractant (I-TAC), and monokine induced by γ interferon (MIG). CEO also significantly inhibited tissue remodelling protein molecules, namely, collagen-I, collagen-III, macrophage colony-stimulating factor (M-CSF), and tissue inhibitor of metalloproteinase 2 (TIMP-2). Furthermore, it significantly modulated global gene expression and altered signalling pathways critical for inflammation, tissue remodelling, and cancer signalling processes. CEO significantly inhibited VCAM-1 and collagen III at both protein and gene expression levels.Conclusions: This study provides important evidence of CEO-induced anti-inflammatory and tissue remodelling activity in human dermal fibroblasts. This study also supports the anticancer properties of CEO and its major active component eugenol.

The effect of cinnamon (Cinnamomum zeylanicum) bark essential oil (CBEO) on human skin cells has not been elucidated. Therefore, we investigated the activity of a commercially available CBEO in a validated human dermal fibroblast system, a model of chronic inflammation and fibrosis. We first evaluated the impact of CBEO on 17 protein biomarkers that play critical roles in inflammation and tissue remodeling. The impact of CBEO on genome‐wide gene expression was also evaluated. CBEO showed strong anti‐proliferative effects on skin cells and significantly inhibited the production of several inflammatory biomarkers, including vascular cell adhesion molecule‐1, intercellular cell adhesion molecule‐1, monocyte chemoattractant protein‐1, interferon gamma‐induced protein 10, interferon‐inducible T‐cell alpha chemoattractant, and monokine induced by gamma interferon. In addition, CBEO significantly inhibited the production of several tissue remodeling molecules, including epidermal growth factor receptor, matrix metalloproteinase‐1, and plasminogen activator inhibitor‐1. Macrophage colony‐stimulating factor, which is an immunomodulatory protein molecule, was also significantly inhibited by CBEO. Furthermore, CBEO significantly modulated global gene expression and altered signaling pathways, many of which are important in inflammation, tissue remodeling, and cancer biology. The study shows that CBEO is a promising antiinflammatory agent; however, further research is required to clarify its clinical efficacy. © 2017 The Authors. Phytotherapy Research published by John Wiley & Sons Ltd.

Research on the biological effects of essential oils on human skin cells is scarce. In the current study, we primarily explored the biological activities of 10 essential oils (nine single and one blend) in a pre-inflamed human dermal fibroblast system that simulated chronic inflammation. We measured levels of proteins critical for inflammation, immune responses, and tissue-remodeling processes. The nine single oils were distilled from Citrus bergamia (bergamot), Coriandrum sativum (cilantro), Pelargonium graveolens (geranium), Helichrysum italicum (helichrysum), Pogostemon cablin (patchouli), Citrus aurantium (petitgrain), Santalum album (sandalwood), Nardostachys jatamansi (spikenard), and Cananga odorata (ylang ylang). The essential oil blend (commercial name Immortelle) is composed of oils from frankincense, Hawaiian sandalwood, lavender, myrrh, helichrysum, and rose. All the studied oils were significantly anti-proliferative against these cells. Furthermore, bergamot, cilantro, and spikenard essential oils primarily inhibited protein molecules related to inflammation, immune responses, and tissue-remodeling processes, suggesting they have anti-inflammatory and wound healing properties. Helichrysum and ylang ylang essential oils, as well as Immortelle primarily inhibited tissue remodeling-related proteins, suggesting a wound healing property. The data are consistent with the results of existing studies examining these oils in other models and suggest that the studied oils may be promising therapeutic candidates. Further research into their biological mechanisms of action is recommended. The differential effects of these essential oils suggest that they exert activities by different mechanisms or pathways, warranting further investigation. The chemical composition of these oils was analyzed using gas chromatography–mass spectrometry.

The use of oregano (Origanum vulgare) essential oil (OEO) has become popular in skin care products. However, scientific research regarding its effects on human skin cells is scarce. In this study, we investigated the biological activity of a commercially available OEO, which is high in carvacrol content, in a human skin cell disease model. OEO induced marked antiproliferative effects and significantly inhibited several inflammatory biomarkers, including monocyte chemoattractant protein 1 (MCP-1), vascular cell adhesion molecule 1 (VCAM-1), intracellular cell adhesion molecule 1 (ICAM-1), interferon gamma-induced protein 10 (IP-10), interferon-inducible T-cell alpha chemoattractant (I-TAC), and monokine induced by gamma interferon (MIG). OEO also significantly inhibited tissue remodeling biomarkers, namely collagen I, collagen III, epidermal growth factor receptor (EGFR), matrix metalloproteinase 1 (MMP-1), plasminogen activator inhibitor 1 (PAI-1), tissue inhibitor of metalloproteinase (TIMP) 1 and 2. An immunomodulatory biomarker, macrophage colony-stimulating factor (M-CSF), was also strongly inhibited by OEO treatment. In addition, OEO significantly modulated global gene expression and altered signaling pathways, many of which are critical in inflammation, tissue remodeling, and cancer signaling processes. These findings along with existing studies largely support the anti-inflammatory, tissue remodeling, immunomodulatory, and anticancer activities of OEO. In conclusion, this study provides the first evidence of the biological activity of OEO in human dermal fibroblasts. We suggest that OEO, with carvacrol as the major active component, is a promising candidate for use in skin care products with anti-inflammatory and anticancer properties.

The serine chemoreceptor of Escherichia coli contains four canonical methylation sites for sensory adaptation that lie near intersubunit helix interfaces of the Tsr homodimer. An unexplored fifth methylation site, E502, lies at an intrasubunit helix interface closest to the HAMP domain that controls input-output signaling in methyl-accepting chemotaxis proteins. We analyzed, with in vivo Förster resonance energy transfer (FRET) kinase assays, the serine thresholds and response cooperativities of Tsr receptors with different mutationally imposed modifications at sites 1 to 4 and/or at site 5. Tsr variants carrying E or Q at residue 502, in combination with unmodifiable D and N replacements at adaptation sites 1 to 4, underwent both methylation and demethylation/deamidation, although detection of the latter modifications required elevated intracellular levels of CheB. These Tsr variants could not mediate a chemotactic response to serine spatial gradients, demonstrating that adaptational modifications at E502 alone are not sufficient for Tsr function. Moreover, E502 is not critical for Tsr function, because only two amino acid replacements at this residue abrogated serine chemotaxis: Tsr-E502P had extreme kinase-off output and Tsr-E502I had extreme kinase-on output. These large threshold shifts are probably due to the unique HAMP-proximal location of methylation site 5. However, a methylation-mimicking glutamine at any Tsr modification site raised the serine response threshold, suggesting that all sites influence signaling by the same general mechanism, presumably through changes in packing stability of the methylation helix bundle. These findings are consistent with control of input-output signaling in Tsr through dynamic interplay of the structural stabilities of the HAMP and methylation bundles. Motile bacteria detect and follow gradients of attractant and repellent chemicals through chemotaxis signaling pathways (recently reviewed in references 1, 2, and 3). The well-studied chemotaxis machinery of Escherichia coli employs chemoreceptors known as methyl-accepting chemotaxis proteins (MCPs) to regulate the autophosphorylation activity of a cytoplasmic histidine kinase, CheA. A small cytoplasmic protein, CheW, couples CheA to receptor control. Ternary receptor signaling complexes form arrays at the cell poles that produce large changes in CheA activity in response to small changes in chemoeffector concentration. CheA in turn donates its phosphoryl groups to two cytoplasmic response regulators, CheY and CheB, to control rotation of the cell's flagellar motors and a sensory adaptation process, respectively. Phosphorylation of CheY promotes clockwise (CW) motor rotation; phosphorylation of CheB augments its receptormodifying enzymatic activity, demethylation or deamidation of specific MCP residues. Another cytoplasmic enzyme, CheR, is responsible for methylating receptor modification sites. The interplay of CheR and CheB activities regulates the receptor methylation state to offset signaling responses to ambient che...