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Clinical Trial
. 2017 Jun;5(2):190-199.
doi: 10.1002/iid3.153. Epub 2017 Mar 30.

Honey is potentially effective in the treatment of atopic dermatitis: Clinical and mechanistic studies

Abdullah A Alangari  1 , Keith Morris  2 , Bashir A Lwaleed  3 , Laurie Lau  4 , Ken Jones  2 , Rose Cooper  2 , Rowena Jenkins  2
Affiliations
Clinical Trial

Honey is potentially effective in the treatment of atopic dermatitis: Clinical and mechanistic studies

Abdullah A Alangari et al. Immun Inflamm Dis. 2017 Jun.

Abstract

Introduction: As manuka honey (MH) exhibits immunoregulatory and anti-staphylococcal activities, we aimed to investigate if it could be effective in the treatment of atopic dermatitis (AD).

Methods: Adult volunteers with bilateral AD lesions were asked to apply MH on one site overnight for seven consecutive days and leave the contralateral site untreated as possible. Three Item Severity score was used to evaluate the response. Skin swabs were obtained from both sites before and after treatment to investigate the presence of staphylococci and enterotoxin production. In addition, the ability of MH and its methanolic and hexane extracts to down regulate IL4-induced CCL26 protein release from HaCaT cells was evaluated by enzyme linked immunosorbent assay. Also, the ability of MH to modulate calcium ionophore-induced mast cell degranulation was assessed by enzyme immunoassay.

Results: In 14 patients, AD lesions significantly improved post MH treatment versus pre-treatment as compared to control lesions. No significant changes in the skin staphylococci were observed after day 7, irrespective of honey treatment. Consistent with the clinical observation, MH significantly down regulated IL4-induced CCL26 release from HaCaT cells in a dose-dependent manner. This effect was partially lost, though remained significant, when methanolic and hexane extracts of MH were utilized. In addition, mast cell degranulation was significantly inhibited following treatment with MH.

Conclusions: MH is potentially effective in the treatment of AD lesions based on both clinical and cellular studies through different mechanisms. This needs to be confirmed by randomized and controlled clinical trials.

Keywords: Atopic dermatitis; honey; keratinocytes; manuka; mast cells.

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Figures

Figure 1
Figure 1
Three Item Severity (TIS) score of MH treated and control sites pre‐ and post‐treatment. The mean TIS for sites treated with MH was significantly lower than that prior to treatment. n.s, not significant.
Figure 2
Figure 2
HaCaT cells viability after treatment with different concentrations of honey (w/v) using MTS assay. Y‐axis indicates absorbance reading. Bars represent the Mean ± SD. (n = 3). H, honey.
Figure 3
Figure 3
Effect of 1% honey pre‐treatment of HaCaTs on (a) IL4‐induced CCL26 protein release, and (b) m‐RNA expression (GAPDH was used as house keeping gene); (c) IL4‐induced IL8 protein release, and (d) m‐RNA expression (GAPDH was used as house keeping gene). Bars represent the Mean ± SD. (n = 3). H, honey; n.s, not significant.
Figure 4
Figure 4
(a) Western Blotting showing no visible effect of pretreatment of HaCaTs with 1% honey on IL4‐induced STAT6 phosphorylation. (b) Densitometry analysis of p‐STAT6/STAT6 ratio. Bars represent the Mean ± SD. (n = 3). M, medium; H, honey; n.s, not significant.
Figure 5
Figure 5
Effect of pre‐treatment with 1% honey, 1% honey methanol extract, and 1% honey hexane extract on IL4‐induced CCL26 release from HaCaTs. Bars represent the Mean ± SD. (n = 3). H, honey.
Figure 6
Figure 6
Histamine inhibition assay showing dose‐dependent inhibition of LAD‐2 mast cell histamine release by Medihoney™. Bars represent the Mean ± SD. (n = 3). H, honey.
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