Oral administration of royal jelly inhibits the development of atopic dermatitis-like skin lesions in NC/Nga mice.
We have shown previously that in addition to IL-4, IL-5 and IL-10, antigen-specific interferon-gamma (IFN-gamma) production by spleen cells from ovalbumin (OVA)/Alum-immunized mice is inhibited by the administration of royal jelly (RJ). Since it has been shown that both Th1 and Th2 cytokines play pathogenic roles in the generation of atopic dermatitis (AD), we have examined whether RJ suppresses the development of AD-like skin lesions in NC/Nga mice induced by repeated application of picryl chloride (PiCl) under specific pathogen-free (SPF) conditions. Oral administration of RJ to the PiCl-treated NC/Nga mice inhibited the development of AD-like skin lesions in these mice as exemplified by the significant decrease in the total skin severity scores and the decrease in hypertrophy, hyperkeratosis, and infiltration of the epidermis and corium by inflammatory cells. IFN-gamma production by spleen cells from PiCl-treated NC/Nga mice in response to TNP-KLH was partially but significantly inhibited by the oral administration of RJ, while IFN-gamma production by Con A-stimulated spleen cells was not affected. Since inducible nitric oxide (NO) synthase (iNOS)-derived NO has been suggested as an important immunoregulatory mediator in inflammatory autoimmune diseases, we have also examined the expression of iNOS in the dorsal skin lesions of PiCl-treated NC/Nga mice. Interestingly, the expression of iNOS was significantly increased in the skin lesions of RJ-administered mice compared with those of control PBS-administered mice. Thus, our results suggest that RJ suppresses the development of AD-like skin lesions in PiCl-treated NC/Nga mice, possibly by a combination of down-regulating TNP-specific IFN-gamma production and up-regulating iNOS expression.
Taniguchi
Yoshifumi
Y
Fujisaki Institute, Hayashibara Biochemical Laboratories, Inc, Fujisaki 675-1, Okayama 702-8006, Japan.
Kohno
Keizo
K
Inoue
Shin-ichiro
S
Koya-Miyata
Satomi
S
Okamoto
Iwao
I
Arai
Norie
N
Iwaki
Kanso
K
Ikeda
Masao
M
Kurimoto
Masashi
M
D000276:Adjuvants, Immunologic / Q000008:administration & dosage / Q000627:therapeutic use*; D000284:Administration, Oral; D000818:Animals; D003876:Dermatitis, Atopic / Q000139:chemically induced / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D003877:Dermatitis, Contact / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D003875:Drug Eruptions / Q000209:etiology / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D004353:Drug Evaluation, Preclinical; D005227:Fatty Acids / Q000008:administration & dosage / Q000627:therapeutic use*; D005260:Female; D006241:Haptens / Q000633:toxicity; D006984:Hypertrophy; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D051379:Mice; D008817:Mice, Mutant Strains; D019001:Nitric Oxide Synthase / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II; D010853:Picryl Chloride / Q000633:toxicity; D012867:Skin / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D013047:Specific Pathogen-Free Organisms; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology; D000099219:Royal Jelly
D000276:Adjuvants, Immunologic; D005227:Fatty Acids; D006241:Haptens; D007073:Immunoglobulin E; D007074:Immunoglobulin G; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D010853:Picryl Chloride; D000099219:Royal Jelly; C496317:Nos2 protein, mouse