title: Interleukin-17/T-helper 17 cells in an atopic dermatitis mouse model aggravate orthodontic root resorption in dental pulp.
abstract: Interleukin (IL)-17 is an important mediator of orthodontically induced inflammatory root resorption (OIIRR). However, its role in the dental pulp (DP) has not been studied. The aim of this study was to investigate, using an atopic dermatitis (AD) model, how IL-17 contributes to OIIRR in DP. Atopic dermatitis is the most common IL-17-associated allergic disease. Atopic dermatitis model mice (AD group) and wild-type mice (control group) were subjected to an excessive orthodontic force. The localization of T-helper (Th)17 cells, IL-17, IL-6, and keratinocyte chemoattractant (KC; an IL-8-related protein in rodents) were determined in DP. In addition, CD4+ T cells, including IL-17 production cells, were obtained from patients with AD and from healthy donors, and the effects of IL-17 on the production of IL-6 and IL-8 were investigated using a co-culture of CD4+ T cells with human dental pulp (hDP) cells stimulated with substance P (SP). Immunoreactivity for Th17 cells, IL-17, IL-6, and KC was increased in DP tissue subjected to orthodontic force in the AD group compared with DP tissue subjected to orthodontic force in the control group. The cells obtained from the AD patients displayed increased IL-6 and IL-8 production. These results suggest that IL-17 may aggravate OIIRR in DP.
authors.affiliation: Department of Orthodontics, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
authors.forename: Mami
authors.initials: M
authors.lastname: Shimizu
authors.forename: Masaru
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: Shoji
authors.initials: S
authors.lastname: Fujita
authors.forename: Tadahiko
authors.initials: T
authors.lastname: Utsunomiya
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Kazutaka
authors.initials: K
authors.lastname: Kasai
mesh_terms: D000293:Adolescent; D000328:Adult; D000818:Animals; D015496:CD4-Positive T-Lymphocytes; D002478:Cells, Cultured; D018920:Coculture Techniques; D003782:Dental Pulp; D003876:Dermatitis, Atopic / Q000139:chemically induced*; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D020381:Interleukin-17 / Q000009:adverse effects / Q000097:blood / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008297:Male; D051379:Mice; D060888:Real-Time Polymerase Chain Reaction; D053722:Receptors, Interleukin-17 / Q000097:blood / Q000378:metabolism*; D012391:Root Resorption / Q000209:etiology*; D013373:Substance P; D058504:Th17 Cells / Q000378:metabolism*; D014087:Tooth Movement Techniques / Q000009:adverse effects*
chemical_list: D020381:Interleukin-17; D015850:Interleukin-6; D016209:Interleukin-8; D053722:Receptors, Interleukin-17; D013373:Substance P; D007073:Immunoglobulin E