title: Oral administration of acarbose ameliorates imiquimod-induced psoriasis-like dermatitis in a mouse model.
abstract: Psoriasis is a chronic autoimmune disease of undefined etiology that involves dysregulated interplay between immune cells and keratinocytes. Acarbose was found to decrease inflammatory parameters in diabetic patients in addition to its anti-diabetic effects. Here, we report that imiquimod (IMQ)-induced epidermal hyperplasia and psoriasis like-inflammation were significantly inhibited by acarbose treatment. Real-time PCR showed that mRNA levels of the cytokines TNF-α, IL-6, IL-1β IL-17A, and IL-22 in skin were also decreased significantly by acarbose. In addition, we found that acarbose reduced infiltration of CD3(+) T cells and GR-1(+) neutrophils in lesional skin and also reduced the percentage of IL-17-producing CD4(+) T cells (Th17) and IL-17- and IL-22-producing γδ T cells in the spleen. In contrast, acarbose increased the frequency of IL-10-producing CD4(+) regulator Tr1 T cells in the spleen and small intestine. These results indicate that oral administration of acarbose can attenuate the severity of imiquimod-induced psoriasis with local and systemic anti-inflammatory and immune modulation effects, thus suggesting that acarbose is an effective therapeutic strategy for psoriasis regulation.
authors.affiliation: Institute of Biomedical Science and Rong Hsing Research Center for Translational Medicine, Chung-Hsing University, Taichung, Taiwan; Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan; School of Medicine, National Yang-Ming University, Taipei, Taiwan; Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan; School of Medicine, Chung-Shan Medical University, Taichung, Taiwan; Institute of Public Health and Community Medicine Research Center, National Yang-Ming University, Taiwan.
authors.forename: Hsin-Hua
authors.initials: HH
authors.lastname: Chen
authors.affiliation: Institute of Biomedical Science and Rong Hsing Research Center for Translational Medicine, Chung-Hsing University, Taichung, Taiwan.
authors.forename: Ya-Hsuan
authors.initials: YH
authors.lastname: Chao
authors.affiliation: Institute of Biomedical Science and Rong Hsing Research Center for Translational Medicine, Chung-Hsing University, Taichung, Taiwan; Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan; School of Medicine, National Yang-Ming University, Taipei, Taiwan; Division of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan; School of Medicine, Chung-Shan Medical University, Taichung, Taiwan.
authors.forename: Der-Yuan
authors.initials: DY
authors.lastname: Chen
authors.affiliation: Division of Rheumatology/Immunology/Allergy, Department of Internal Medicine, Taichung Armed Forces General Hospital, Taichung, Taiwan.
authors.forename: Deng-Ho
authors.initials: DH
authors.lastname: Yang
authors.affiliation: Department of Medical Science and Institute of Bioinformatics and Structural Biology, National Tsing Hua University, Hsinchu, Taiwan.
authors.forename: Ting-Wen
authors.initials: TW
authors.lastname: Chung
authors.affiliation: Institute of Biomedical Science and Rong Hsing Research Center for Translational Medicine, Chung-Hsing University, Taichung, Taiwan.
authors.forename: Yi-Rong
authors.initials: YR
authors.lastname: Li
authors.affiliation: Institute of Biomedical Science and Rong Hsing Research Center for Translational Medicine, Chung-Hsing University, Taichung, Taiwan; Department of Medical Research, Taichung Veterans General Hospital, Taichung, Taiwan. Electronic address: lincc@dragon.nchu.edu.tw.
authors.forename: Chi Chen
authors.initials: CC
authors.lastname: Lin
mesh_terms: D020909:Acarbose / Q000494:pharmacology / Q000627:therapeutic use*; D000284:Administration, Oral; D000634:Aminoquinolines; D000818:Animals; D002465:Cell Movement / Q000187:drug effects; D016207:Cytokines / Q000378:metabolism; D003877:Dermatitis, Contact / Q000188:drug therapy*; D004195:Disease Models, Animal; D006801:Humans; D000077271:Imiquimod; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology; D011565:Psoriasis / Q000139:chemically induced / Q000188:drug therapy*; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000378:metabolism; D012867:Skin / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000276:immunology; D058504:Th17 Cells / Q000187:drug effects* / Q000276:immunology
chemical_list: D000634:Aminoquinolines; D016207:Cytokines; D016692:Receptors, Antigen, T-Cell, gamma-delta; D000077271:Imiquimod; D020909:Acarbose
keywords: Acarbose; IL-10; Imiquimod; Inflammation; Psoriasis; Tr1 T cells