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Increased scratching counts depend on a decrease in ability of cutaneous prostaglandin D2 biosynthesis in NC/Nga mice with atopic dermatitis.
Exp Dermatol. 2005 Dec; 14(12):898-905.ED

Abstract

Spontaneous and 2,4,6-trinitrochlorobenzene (TNCB)-induced dermatitis models using NC/Nga mice have been recognized as animal models of atopic dermatitis. We reported that scratching behavior leads to dermatitis in a spontaneous dermatitis but not in a TNCB-induced dermatitis. Prostaglandin D2 (PGD2) suppressed the scratching behavior of NC/Nga mice, suggesting that PGD2 plays a physiological role on inhibiting pruritus. We studied whether there was a difference in skin PG contents between spontaneous and TNCB-induced dermatitis. Spontaneous dermatitis was induced by cohabitation with NC/Nga mice having severe skin lesions. TNCB-induced dermatitis was caused by applications of TNCB. PGD2, PGE2, 6keto-PGF1alpha, and PGF2alpha contents in the skin were examined using enzyme-immunoassay kits. For studying ability to produce skin PGs, PG contents were evaluated after topical treatment of arachidonic acid (AA) or mechanical scratching. In spontaneous dermatitis, PGE2, 6keto-PGF1alpha, and PGF2alpha contents increased with dermatitis, but only PGD2 did not do so. In TNCB-induced dermatitis, PGD2, PGE2, 6keto-PGF1alpha, and PGF2alpha increased. Determination of skin PG contents after AA treatment or mechanical scratching revealed that skin PGD2 production of conventional group of spontaneous dermatitis was lower than the specific pathogen-free group. It seemed that ability of skin PGD2 production was attenuated in spontaneous dermatitis. These results suggest that enhancement of scratching behavior in spontaneous dermatitis was caused by the defect of ability to produce PGD2, which plays a physiological role in inhibiting pruritus, resulting in development of dermatitis.

Authors+Show Affiliations

Department of Pharmacology, Medicinal Research Laboratories, Taisho Pharmaceutical Co. Ltd, Saitama, Japan. masanori.sugimoto@po.rd.taisho.co.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16274457

Citation

Sugimoto, M, et al. "Increased Scratching Counts Depend On a Decrease in Ability of Cutaneous Prostaglandin D2 Biosynthesis in NC/Nga Mice With Atopic Dermatitis." Experimental Dermatology, vol. 14, no. 12, 2005, pp. 898-905.
Sugimoto M, Arai I, Futaki N, et al. Increased scratching counts depend on a decrease in ability of cutaneous prostaglandin D2 biosynthesis in NC/Nga mice with atopic dermatitis. Exp Dermatol. 2005;14(12):898-905.
Sugimoto, M., Arai, I., Futaki, N., Hashimoto, Y., Honma, Y., & Nakaike, S. (2005). Increased scratching counts depend on a decrease in ability of cutaneous prostaglandin D2 biosynthesis in NC/Nga mice with atopic dermatitis. Experimental Dermatology, 14(12), 898-905.
Sugimoto M, et al. Increased Scratching Counts Depend On a Decrease in Ability of Cutaneous Prostaglandin D2 Biosynthesis in NC/Nga Mice With Atopic Dermatitis. Exp Dermatol. 2005;14(12):898-905. PubMed PMID: 16274457.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased scratching counts depend on a decrease in ability of cutaneous prostaglandin D2 biosynthesis in NC/Nga mice with atopic dermatitis. AU - Sugimoto,M, AU - Arai,I, AU - Futaki,N, AU - Hashimoto,Y, AU - Honma,Y, AU - Nakaike,S, PY - 2005/11/9/pubmed PY - 2006/1/4/medline PY - 2005/11/9/entrez SP - 898 EP - 905 JF - Experimental dermatology JO - Exp Dermatol VL - 14 IS - 12 N2 - Spontaneous and 2,4,6-trinitrochlorobenzene (TNCB)-induced dermatitis models using NC/Nga mice have been recognized as animal models of atopic dermatitis. We reported that scratching behavior leads to dermatitis in a spontaneous dermatitis but not in a TNCB-induced dermatitis. Prostaglandin D2 (PGD2) suppressed the scratching behavior of NC/Nga mice, suggesting that PGD2 plays a physiological role on inhibiting pruritus. We studied whether there was a difference in skin PG contents between spontaneous and TNCB-induced dermatitis. Spontaneous dermatitis was induced by cohabitation with NC/Nga mice having severe skin lesions. TNCB-induced dermatitis was caused by applications of TNCB. PGD2, PGE2, 6keto-PGF1alpha, and PGF2alpha contents in the skin were examined using enzyme-immunoassay kits. For studying ability to produce skin PGs, PG contents were evaluated after topical treatment of arachidonic acid (AA) or mechanical scratching. In spontaneous dermatitis, PGE2, 6keto-PGF1alpha, and PGF2alpha contents increased with dermatitis, but only PGD2 did not do so. In TNCB-induced dermatitis, PGD2, PGE2, 6keto-PGF1alpha, and PGF2alpha increased. Determination of skin PG contents after AA treatment or mechanical scratching revealed that skin PGD2 production of conventional group of spontaneous dermatitis was lower than the specific pathogen-free group. It seemed that ability of skin PGD2 production was attenuated in spontaneous dermatitis. These results suggest that enhancement of scratching behavior in spontaneous dermatitis was caused by the defect of ability to produce PGD2, which plays a physiological role in inhibiting pruritus, resulting in development of dermatitis. SN - 0906-6705 UR - https://www.unboundmedicine.com/medline/citation/16274457/Increased_scratching_counts_depend_on_a_decrease_in_ability_of_cutaneous_prostaglandin_D2_biosynthesis_in_NC/Nga_mice_with_atopic_dermatitis_ L2 - https://doi.org/10.1111/j.1600-0625.2005.00375.x DB - PRIME DP - Unbound Medicine ER -