title: Topical application of Pleurotus eryngii extracts inhibits 2,4-dinitrochlorobenzene-induced atopic dermatitis in NC/Nga mice by the regulation of Th1/Th2 balance.
abstract: Pleurotus eryngii is a nutritional and medicinal food rich in polysaccharides that enhance the host immune system as a response to various diseases. The present study investigated the effects of P. eryngii extracts (PEE) on the progress of atopic dermatitis (AD)-like skin lesions in NC/Nga mice induced by 2,4-dinitrochlorobenzene (DNCB). We evaluated skin dermatitis severity, ear thickness, histopathological examination, and cytokines level in DNCB-applied mice treated with PEE. Continuous treatment of PEE inhibited the development of the AD-like skin lesions. PEE suppressed DNCB-induced dermatitis severity, serum level of IgE and thymus and activation-regulated chemokine (TARC), and mRNA expression of TNF-α, INF-γ, IL-4, IL-5, and IL-13 in mice. In addition, PEE reduced thickness of the dermis and dermal infiltration of inflammatory cells and mast cells in histopathological examination. These results indicate that PEE inhibits allergic contact dermatitis through the modulating of T helper (Th)1 and Th2 responses and diminishing the inflammatory cells and mast cells infiltration in the skin lesions in NC/Nga mice.
authors.affiliation: Department of Toxicology, College of Pharmacy, Chungnam National University, Daejeon 305-764, Republic of Korea.
authors.forename: Jae Ho
authors.initials: JH
authors.lastname: Choi
authors.forename: Hyung Gyun
authors.initials: HG
authors.lastname: Kim
authors.forename: Sun Woo
authors.initials: SW
authors.lastname: Jin
authors.forename: Eun Hee
authors.initials: EH
authors.lastname: Han
authors.forename: Tilak
authors.initials: T
authors.lastname: Khanal
authors.forename: Minh Truong
authors.initials: MT
authors.lastname: Do
authors.forename: Yong Pil
authors.initials: YP
authors.lastname: Hwang
authors.forename: Jun Min
authors.initials: JM
authors.lastname: Choi
authors.forename: Sung-Sik
authors.initials: SS
authors.lastname: Chun
authors.forename: Young Chul
authors.initials: YC
authors.lastname: Chung
authors.forename: Tae Cheon
authors.initials: TC
authors.lastname: Jeong
authors.forename: Hye Gwang
authors.initials: HG
authors.lastname: Jeong
mesh_terms: D000818:Animals; D054414:Chemokine CCL17 / Q000097:blood; D003876:Dermatitis, Atopic / Q000139:chemically induced / Q000188:drug therapy* / Q000473:pathology; D004137:Dinitrochlorobenzene / Q000009:adverse effects*; D007073:Immunoglobulin E / Q000097:blood; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D018793:Interleukin-13 / Q000235:genetics / Q000378:metabolism; D015847:Interleukin-4 / Q000235:genetics / Q000378:metabolism; D015848:Interleukin-5 / Q000235:genetics / Q000378:metabolism; D008297:Male; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D020076:Pleurotus; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D058408:Th1-Th2 Balance / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D054414:Chemokine CCL17; D004137:Dinitrochlorobenzene; D018793:Interleukin-13; D015848:Interleukin-5; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; D007073:Immunoglobulin E; D007371:Interferon-gamma