Reduction of nickel-induced contact hypersensitivity reactions by topical tea tree oil in humans.

OBJECTIVE AND DESIGN: Whilst the anti-microbial properties of tea tree oil (TTO) are established, the anti-inflammatory effects of TTO in human skin remain largely anecdotal and require evaluation. This study examined the effect of topically applied TTO on nickel-induced contact hypersensitivity reactions in human dorsal skin. TREATMENT: TTO (100%), a 5% TTO lotion, a placebo lotion (no TTO), or 100% macadamia oil were applied at days 3 and 5 after nickel exposure. METHODS: The flare area and erythema index were measured on days 3, 5 and 7. The regulatory effects of TTO were also investigated on the proliferative response to nickel or polyclonal mitogens by peripheral blood mononuclear cells from nickel-sensitive and control subjects. RESULTS: TTO (100%) significantly reduced the flare area and erythema index when compared to the nickel-only sites. With respect to the erythema index, the anti-inflammatory effects were predominantly, but not exclusively, seen in a subgroup of nickel-sensitive subjects with a prolonged development phase of nickel-induced contact hypersensitivity response. The 5% TTO lotion, the placebo lotion and the 100% macadamia oil were all without significant effect. TTO significantly inhibited proliferation to nickel but not to non-specific polyclonal mitogens by peripheral blood mononuclear cells from nickel-sensitive subjects. CONCLUSIONS: Topical application of 100% TTO may have therapeutic benefit in nickel-induced contact hypersensitivity in human skin. The mode of action of TTO requires further investigation, but may be an effect on the antigen presenting cells or the antigen presenting process in nickel-induced contact hypersensitivity, as well as vascular changes associated with this response.

Tea tree oil reduces histamine-induced skin inflammation.

BACKGROUND: Tea tree oil is the essential oil steam-distilled from Melaleuca alternifolia, an Australian native plant. In recent years it has become increasingly popular as an antimicrobial for the treatment of conditions such as tinea pedis and acne. OBJECTIVES: To investigate the anti-inflammatory properties of tea tree oil on histamine-induced weal and flare. METHODS: Twenty-seven volunteers were injected intradermally in each forearm (study and control assigned on an alternating basis) with histamine diphosphate (5 microg in 50 microL). Flare and weal diameters and double skin thickness were measured every 10 min for 1 h to calculate flare area and weal volume. At 20 min, 25 microL of 100% tea tree oil was applied topically to the study forearm of 21 volunteers. For six volunteers, 25 microL paraffin oil was applied instead of tea tree oil. RESULTS: Application of liquid paraffin had no significant effect on histamine-induced weal and flare. There was also no difference in mean flare area between control arms and those on which tea tree oil was applied. However, mean weal volume significantly decreased after tea tree oil application (10 min after tea tree oil application, P = 0.0004, Mann-Whitney U-test). CONCLUSIONS: This is the first study to show experimentally that tea tree oil can reduce histamine-induced skin inflammation.

Tea tree oil reduces the swelling associated with the efferent phase of a contact hypersensitivity response.

OBJECTIVE: To examine the anti-inflammatory activities of tea tree oil (TTO) in vivo. METHODS: Mice were sensitized to a chemical hapten, trinitrochlorobenzene, on their ventral skin and 7 days later challenged (or re-exposed) on their dorsal skin with the same hapten. RESULTS: TTO applied 30 min before or up to 7 h after to the same dorsal site as hapten challenge caused a significant reduction in skin swelling after 24 h. TTO reduced oedema but not the influx of inflammatory cells. This finding was supported by the inability of TTO to suppress TNFalpha-induced E-selectin expression by human umbilical vein endothelial cells. TTO did not suppress irritant- or ultraviolet B-induced oedema. CONCLUSION: Topical TTO, specifically the TTO components, terpinen-4-ol and alpha-terpineol can regulate the oedema associated with the efferent phase of a contact hypersensitivity response.

Tea tree oil reduces histamine-induced oedema in murine ears.

OBJECTIVE: To examine the effect of topically applied tea tree oil (TTO) on histamine-induced oedema in the ears of mice. METHODS AND RESULTS: For BALB/c mice, 10 microl undiluted TTO applied immediately after, but not 30 min before intradermal injection of 600 microg histamine in 10 microl, significantly suppressed oedema development. TTO applied after histamine injection also suppressed histamine-induced oedema in C57/BL6 mice. TTO applied immediately after intradermal injection of compound 48/80 (200 microg in 10 microl saline) also significantly reduced ear swelling. TTO suppressed histamine-induced oedema to the same extent in capsaicin-treated (neuropeptide-depleted) and control mice which suggests that TTO does not inhibit histamine-induced oedema by regulating the activity of peripheral sensory neurons. Terpinen-4-ol, the major water-soluble component of TTO, was equivalent in potency to TTO in the suppression of histamine-induced ear swelling. CONCLUSION: Topical application of TTO, and in particular terpinen-4-ol, may be effective in controlling histamine-induced oedema often associated with Type I allergic immediate hypersensitivities.

The water-soluble components of the essential oil of Melaleuca alternifolia (tea tree oil) suppress the production of superoxide by human monocytes, but not neutrophils, activated in vitro.

OBJECTIVE: To evaluate the regulatory properties of the essential oil of Melaleuca alternifolia (tea tree oil) on the production of oxygen derived reactive species by human peripheral blood leukocytes activated in vitro. MATERIALS AND METHODS: The ability of tea tree oil to reduce superoxide production by neutrophils and monocytes stimulated with N-formyl-methionyl-leucyl-phenylalanine (fMLP), lipopolysaccharide (LPS) or phorbol 12-myristate 13-acetate (PMA) was examined. RESULTS: The water-soluble fraction of tea tree oil had no significant effect on agonist-stimulated superoxide production by neutrophils, but significantly and dose-dependently suppressed agonist-stimulated superoxide production by monocytes. This suppression was not due to cell death. Chemical analysis identified the water-soluble components to be terpinen-4-ol, alpha-terpineol and 1,8-cineole. When examined individually, terpinen-4-ol significantly suppressed fMLP- and LPS- but not PMA-stimulated superoxide production; alpha-terpineol significantly suppressed fMLP-, LPS- and PMA-stimulated superoxide production; 1,8-cineole was without effect. CONCLUSION: Tea tree oil components suppress the production of superoxide by monocytes, but not neutrophils, suggesting the potential for selective regulation of cell types by these components during inflammation.

Terpinen-4-ol, the main component of the essential oil of Melaleuca alternifolia (tea tree oil), suppresses inflammatory mediator production by activated human monocytes.

OBJECTIVE AND DESIGN: To evaluate potential antiinflammatory properties of tea tree oil, the essential oil steam distilled from the Australian native plant, Melaleuca alternifolia. MATERIAL AND METHODS: The ability of tea tree oil to reduce the production in vitro of tumour necrosis factor-alpha (TNFalpha), interleukin (IL)-1beta, IL-8, IL-10 and prostaglandin E2 (PGE2) by lipopolysaccharide (LPS)-activated human peripheral blood monocytes was examined. RESULTS: Tea tree oil emulsified by sonication in a glass tube into culture medium containing 10% fetal calf serum (FCS) was toxic for monocytes at a concentration of 0.016% v/v. However, the water soluble components of tea tree oil at concentrations equivalent to 0.125% significantly suppressed LPS-induced production of TNFalpha, IL-1beta and IL-10 (by approximately 50%) and PGE2 (by approximately 30%) after 40 h. Gas chromatography/mass spectrometry identified terpinen-4-ol (42 %), a-terpineol (3 %) and 1,8-cineole (2%, respectively, of tea tree oil) as the water soluble components of tea tree oil. When these components were examined individually, only terpinen-4-ol suppressed the production after 40 h of TNFalpha, IL-1beta, IL-8, IL-10 and PGE2 by LPS-activated monocytes. CONCLUSION: The water-soluble components of tea tree oil can suppress pro-inflammatory mediator production by activated human monocytes.