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The histone deacetylase inhibitor, trichostatin A, inhibits the development of 2,4-dinitrofluorobenzene-induced dermatitis in NC/Nga mice.
Int Immunopharmacol. 2010 Oct; 10(10):1310-5.II

Abstract

Repetitive skin contact with a chemical hapten like 2,4-dinitrofluorobenzene (DNFB) evokes an atopic dermatitis (AD)-like dermatitis reaction in NC/Nga mice maintained under specific pathogen-free (SPF) conditions. The histone deacetylase (HDAC) inhibitor, trichostatin A (TSA), modulates the expression of several genes by inhibiting the activity of HDACs. Furthermore, TSA has been reported to suppress inflammatory cytokine expression and to induce T cell-suppression by increasing regulatory T cell (T reg cell) numbers. In addition, histone deacetylase inhibitors (HDACi) are currently undergoing clinical trials for the treatment of inflammatory disorders. In the present study, we examined whether treatment with TSA suppresses AD-like skin lesions in NC/Nga mice treated with DNFB under SPF conditions. Intraperitoneal (i.p.) administration of TSA to DNFB-treated NC/Nga mice was found to inhibit ear thickness increases and the skin lesions induced by DNFB. Furthermore, IL-4 production by CD4+ T cells from the lymph nodes of DNFB-treated NC/Nga mice was significantly inhibited by TSA, although levels of IFN-γ were not. Flow cytometric analysis of lymphocytes showed an increase in CD4+ CD25+ T cell proportions in mice given TSA-i.p. These findings suggest that TSA suppresses the development of AD-like dermatitis in DNFB-treated NC/Nga mice by reducing IL-4 production and increasing the T reg cell population.

Authors+Show Affiliations

Department of Microbiology (BK21), College of Medicine, Kyung Hee University, Seoul 130701, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20728595

Citation

Kim, Tae-Ho, et al. "The Histone Deacetylase Inhibitor, Trichostatin A, Inhibits the Development of 2,4-dinitrofluorobenzene-induced Dermatitis in NC/Nga Mice." International Immunopharmacology, vol. 10, no. 10, 2010, pp. 1310-5.
Kim TH, Jung JA, Kim GD, et al. The histone deacetylase inhibitor, trichostatin A, inhibits the development of 2,4-dinitrofluorobenzene-induced dermatitis in NC/Nga mice. Int Immunopharmacol. 2010;10(10):1310-5.
Kim, T. H., Jung, J. A., Kim, G. D., Jang, A. H., Cho, J. J., Park, Y. S., & Park, C. S. (2010). The histone deacetylase inhibitor, trichostatin A, inhibits the development of 2,4-dinitrofluorobenzene-induced dermatitis in NC/Nga mice. International Immunopharmacology, 10(10), 1310-5. https://doi.org/10.1016/j.intimp.2010.08.004
Kim TH, et al. The Histone Deacetylase Inhibitor, Trichostatin A, Inhibits the Development of 2,4-dinitrofluorobenzene-induced Dermatitis in NC/Nga Mice. Int Immunopharmacol. 2010;10(10):1310-5. PubMed PMID: 20728595.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The histone deacetylase inhibitor, trichostatin A, inhibits the development of 2,4-dinitrofluorobenzene-induced dermatitis in NC/Nga mice. AU - Kim,Tae-Ho, AU - Jung,Jung-A, AU - Kim,Gun-Dong, AU - Jang,An-Hee, AU - Cho,Jeong-Je, AU - Park,Yong Seek, AU - Park,Cheung-Seog, Y1 - 2010/08/20/ PY - 2010/05/14/received PY - 2010/07/14/revised PY - 2010/08/05/accepted PY - 2010/8/24/entrez PY - 2010/8/24/pubmed PY - 2011/2/16/medline SP - 1310 EP - 5 JF - International immunopharmacology JO - Int Immunopharmacol VL - 10 IS - 10 N2 - Repetitive skin contact with a chemical hapten like 2,4-dinitrofluorobenzene (DNFB) evokes an atopic dermatitis (AD)-like dermatitis reaction in NC/Nga mice maintained under specific pathogen-free (SPF) conditions. The histone deacetylase (HDAC) inhibitor, trichostatin A (TSA), modulates the expression of several genes by inhibiting the activity of HDACs. Furthermore, TSA has been reported to suppress inflammatory cytokine expression and to induce T cell-suppression by increasing regulatory T cell (T reg cell) numbers. In addition, histone deacetylase inhibitors (HDACi) are currently undergoing clinical trials for the treatment of inflammatory disorders. In the present study, we examined whether treatment with TSA suppresses AD-like skin lesions in NC/Nga mice treated with DNFB under SPF conditions. Intraperitoneal (i.p.) administration of TSA to DNFB-treated NC/Nga mice was found to inhibit ear thickness increases and the skin lesions induced by DNFB. Furthermore, IL-4 production by CD4+ T cells from the lymph nodes of DNFB-treated NC/Nga mice was significantly inhibited by TSA, although levels of IFN-γ were not. Flow cytometric analysis of lymphocytes showed an increase in CD4+ CD25+ T cell proportions in mice given TSA-i.p. These findings suggest that TSA suppresses the development of AD-like dermatitis in DNFB-treated NC/Nga mice by reducing IL-4 production and increasing the T reg cell population. SN - 1878-1705 UR - https://www.unboundmedicine.com/medline/citation/20728595/The_histone_deacetylase_inhibitor_trichostatin_A_inhibits_the_development_of_24_dinitrofluorobenzene_induced_dermatitis_in_NC/Nga_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1567-5769(10)00247-X DB - PRIME DP - Unbound Medicine ER -