Cutaneous Application of Royal Jelly Inhibits Skin Lesions in NC/Nga Mice, a Human-Like Mouse Model of Atopic Dermatitis
Anti-allergic effects of royal jelly were evaluated in a human-like mouse model of atopic dermatitis. NC/Nga mice were cutaneously applied with royal jelly for 6 weeks. Royal jelly-treated mice exhibited lower levels of serum total immunoglobulin E in comparison with controls. We found that the treatment decreased (11% to the control) expression of mRNA for aquaporin-3, which is involved in the modulation of epidermal hydration. Microarray analysis revealed more than 10-fold changes in the expression of several genes, such as transglutaminase 2, repetin, and keratins. In normal human epidermal keratinocytes, royal jelly extract suppressed interleukin-8 elevation induced by TNF-α and interferon-γ, suggesting direct anti-inflammatory activity in keratinocytes. Collectively, topical application of royal jelly may be useful for amelioration of lesions and inflammation in atopic dermatitis.
<p>[1] Boguniewicz M and Leung DY. “Atopic dermatitis: a disease of altered
skin barrier and immune dysregulation.” Immunol Rev., 242, 2011, pp.
233-246.
[2] Viuda-Martos M, Ruiz-Navajas Y, Fernández-López J and Pérez-Alvarez
JA. “Functional properties of honey, propolis, and royal jelly.” J. Food
Sci., 73, 2008, pp. 117-124.
[3] Oka H, Emori Y, Kobayashi N, Hayashi Y and Nomoto K. “Suppression
of allergic reactions by royal jelly in association with the restoration of
macrophage function and the improvement of Th1/Th2 cell responses.”
Int. Immunopharmacol., 1, 2001, pp. 521–532.
[4] Taniguchi Y, Kohno K, Inoue S, Koya-Miyata S, Okamoto I , Arai N,
Iwaki K, Ikeda M and Kurimoto M. “Oral administration of royal jelly
inhibits the development of atopic dermatitis-like skin lesions in NC/Nga
mice.” Int . Immunopharmacol., 3, 2003, pp. 1313-1324.
[5] Tanabe S and Hochi S. “Oral administration of a galactooligosaccharide
preparation inhibits development of atopic dermatitis-like skin lesions in
NC/Nga mice.” Int. J. Mol. Med., 25, 2010, pp. 331-336.
[6] Olsson M, Broberg A, Jernås M, Carlsson L, Rudemo M, Suurküla M,
Svensson PA and Benson M. “Increased expression of aquaporin 3 in
atopic eczema.” Allergy., 61, 2006, pp. 1132-1137.
[7] Nakahigashi K, Kabashima K, Ikoma A, Verkman AS, Miyachi Y and
Hara-Chikuma M. “Upregulation of aquaporin-3 is involved in
keratinocyte proliferation and epidermal hyperplasia.” J. Invest.
Dermatol., 131, 2011, pp. 865-873.
[8] Kim Y, Eom S, Kim K, Lee YS, Choe J, Hahn JH, Lee H, Kim YM, Ha
KS, Ro JY and Jeoung D. “Transglutaminase II interacts with rac1,
regulates production of reactive oxygen species, expression of snail,
secretion of Th2 cytokines and mediates in vitro and in vivo allergic
inflammation.” Mol. Immunol., 47, 2010, pp. 1010-1022.
[9] Huber M, Siegenthaler G, Mi rancea N, Marenholz I, Nizetic D,
Breitkreutz D, Mischke D and Hohl D. “Isolation and characterization of
human repetin, a member of the fused gene family of the epidermal
differentiation complex.” J. Invest. Dermatol., 124, 2005, pp. 998-1007.
[10] Kim CH, Choi YS, Cheong K and Lee AY. “Mechanism underlying the
effect of combined therapy using glucosamine and low-dose cyclosporine
A on the development of atopic dermatitis-like skin lesions in NC/Nga
mice.” Int. Immunopharmacol., 15, 2013, pp. 424-432.
[11] Theerawatanasirikul S, Sailasuta A, Thanawongnuwech R and
Suriyaphol G. “Alterations of keratins, involucrin and filaggrin gene
expression in canine atopic dermatitis.” Res. Vet. Sci., 93, 2012, pp.
1287-1292.</p>
<p>[1] Boguniewicz M and Leung DY. “Atopic dermatitis: a disease of altered
skin barrier and immune dysregulation.” Immunol Rev., 242, 2011, pp.
233-246.
[2] Viuda-Martos M, Ruiz-Navajas Y, Fernández-López J and Pérez-Alvarez
JA. “Functional properties of honey, propolis, and royal jelly.” J. Food
Sci., 73, 2008, pp. 117-124.
[3] Oka H, Emori Y, Kobayashi N, Hayashi Y and Nomoto K. “Suppression
of allergic reactions by royal jelly in association with the restoration of
macrophage function and the improvement of Th1/Th2 cell responses.”
Int. Immunopharmacol., 1, 2001, pp. 521–532.
[4] Taniguchi Y, Kohno K, Inoue S, Koya-Miyata S, Okamoto I , Arai N,
Iwaki K, Ikeda M and Kurimoto M. “Oral administration of royal jelly
inhibits the development of atopic dermatitis-like skin lesions in NC/Nga
mice.” Int . Immunopharmacol., 3, 2003, pp. 1313-1324.
[5] Tanabe S and Hochi S. “Oral administration of a galactooligosaccharide
preparation inhibits development of atopic dermatitis-like skin lesions in
NC/Nga mice.” Int. J. Mol. Med., 25, 2010, pp. 331-336.
[6] Olsson M, Broberg A, Jernås M, Carlsson L, Rudemo M, Suurküla M,
Svensson PA and Benson M. “Increased expression of aquaporin 3 in
atopic eczema.” Allergy., 61, 2006, pp. 1132-1137.
[7] Nakahigashi K, Kabashima K, Ikoma A, Verkman AS, Miyachi Y and
Hara-Chikuma M. “Upregulation of aquaporin-3 is involved in
keratinocyte proliferation and epidermal hyperplasia.” J. Invest.
Dermatol., 131, 2011, pp. 865-873.
[8] Kim Y, Eom S, Kim K, Lee YS, Choe J, Hahn JH, Lee H, Kim YM, Ha
KS, Ro JY and Jeoung D. “Transglutaminase II interacts with rac1,
regulates production of reactive oxygen species, expression of snail,
secretion of Th2 cytokines and mediates in vitro and in vivo allergic
inflammation.” Mol. Immunol., 47, 2010, pp. 1010-1022.
[9] Huber M, Siegenthaler G, Mi rancea N, Marenholz I, Nizetic D,
Breitkreutz D, Mischke D and Hohl D. “Isolation and characterization of
human repetin, a member of the fused gene family of the epidermal
differentiation complex.” J. Invest. Dermatol., 124, 2005, pp. 998-1007.
[10] Kim CH, Choi YS, Cheong K and Lee AY. “Mechanism underlying the
effect of combined therapy using glucosamine and low-dose cyclosporine
A on the development of atopic dermatitis-like skin lesions in NC/Nga
mice.” Int. Immunopharmacol., 15, 2013, pp. 424-432.
[11] Theerawatanasirikul S, Sailasuta A, Thanawongnuwech R and
Suriyaphol G. “Alterations of keratins, involucrin and filaggrin gene
expression in canine atopic dermatitis.” Res. Vet. Sci., 93, 2012, pp.
1287-1292.</p>
@article{"International Journal of Medical, Medicine and Health Sciences:61130", author = "Junki Miyamoto and Mariko Kiyomi and Yuuki Nagashio and Takuya Suzuki and Soichi Tanabe", title = "Cutaneous Application of Royal Jelly Inhibits Skin Lesions in NC/Nga Mice, a Human-Like Mouse Model of Atopic Dermatitis", abstract = "Anti-allergic effects of royal jelly were evaluated in a human-like mouse model of atopic dermatitis. NC/Nga mice were cutaneously applied with royal jelly for 6 weeks. Royal jelly-treated mice exhibited lower levels of serum total immunoglobulin E in comparison with controls. We found that the treatment decreased (11% to the control) expression of mRNA for aquaporin-3, which is involved in the modulation of epidermal hydration. Microarray analysis revealed more than 10-fold changes in the expression of several genes, such as transglutaminase 2, repetin, and keratins. In normal human epidermal keratinocytes, royal jelly extract suppressed interleukin-8 elevation induced by TNF-α and interferon-γ, suggesting direct anti-inflammatory activity in keratinocytes. Collectively, topical application of royal jelly may be useful for amelioration of lesions and inflammation in atopic dermatitis.
", keywords = "Aquaporin 3, immunoglobulin E, NC/Nga, royal
jelly.", volume = "7", number = "7", pages = "407-4", }
