title: Paeoniflorin inhibits skin lesions in imiquimod-induced psoriasis-like mice by downregulating inflammation.
abstract: Psoriasis is a common chronic immune-mediated inflammatory disease. It is well known that macrophages, neutrophils and T-helper 1 (Th1)/T-helper 17 (Th17) cells play important roles in skin lesions by provoking inflammation. Paeoniflorin (PF) is the major effective component extracted from the root of Paeonia lactiflora, which has been widely used in China to treat inflammatory and autoimmune diseases, including psoriasis. Although PF shows a clinical therapeutic effect on psoriasis patients, how PF affects infiltrated immune cells in psoriasis skin lesions is still unknown. In this study, using a generated imiquimod (IMQ)-induced psoriasis-like mouse model, we found that PF ameliorates inflammation and skin lesions. Subsequent analyses showed that PF decreases the number of F4/80(+)CD68(+) macrophages and their related cytokine production (TNF-α, IL-1β, IL-6, IL-12 and inducible nitric oxide synthase (iNOS)) in the skin of IMQ-challenged mice. Moreover, PF suppresses the number of CD11b(+)Gr-1(+) neutrophils and the expression of macrophage inflammatory protein-2 (MIP-2; a counterpart of human IL-8, which is responsible for the recruitment of neutrophils in mice). Finally, PF also down-regulates Th1- and Th17-related cytokine expression. Therefore, our new findings reveal that PF alleviates psoriatic skin lesions by inhibiting inflammation, which provides new insights into the immunomodulatory effect of PF in psoriasis treatment.
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
authors.forename: Yue
authors.initials: Y
authors.lastname: Sun
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
authors.forename: Jie
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
authors.forename: Rongfen
authors.initials: R
authors.lastname: Huo
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
authors.forename: Tianhang
authors.initials: T
authors.lastname: Zhai
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
authors.forename: Huidan
authors.initials: H
authors.lastname: Li
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
authors.forename: Pinru
authors.initials: P
authors.lastname: Wu
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
authors.forename: Xianjin
authors.initials: X
authors.lastname: Zhu
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
authors.forename: Zhou
authors.initials: Z
authors.lastname: Zhou
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
authors.forename: Baihua
authors.initials: B
authors.lastname: Shen
authors.affiliation: Shanghai Institute of Immunology and Department of Immunology and Microbiology, Institute of medical sciences, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China. Electronic address: ninglixiaoxue57@163.com.
authors.forename: Ningli
authors.initials: N
authors.lastname: Li
mesh_terms: D000634:Aminoquinolines; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D005260:Female; D005960:Glucosides / Q000494:pharmacology* / Q000627:therapeutic use*; D000077271:Imiquimod; D008264:Macrophages / Q000187:drug effects / Q000276:immunology; D008807:Mice, Inbred BALB C; D039821:Monoterpenes / Q000494:pharmacology* / Q000627:therapeutic use*; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D011565:Psoriasis / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D012867:Skin / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D006027:Glycosides
chemical_list: D000634:Aminoquinolines; D000893:Anti-Inflammatory Agents; D016207:Cytokines; D005960:Glucosides; D000077271:Imiquimod; D039821:Monoterpenes; C015423:peoniflorin; D006027:Glycosides
keywords: Cytokine; Imiquimod-induced psoriasis-like mouse model; Inflammatory cells; Paeoniflorin; Skin lesion