title: Suppressive activity of epinastine hydrochloride on TARC production from human peripheral blood CD4+ T cells in-vitro.
abstract: Thymus- and activation-regulated chemokine (TARC) is an important molecule in the development and maintenance of allergic diseases. However, there is little information about the influence of anti-allergic agents on TARC production. The aim of this study is to examine the influence of epinastine hydrochloride, an H1-receptor antagonist, on TARC production from human peripheral blood CD4+ T cells using an in-vitro cell culture technique. CD4+ T cells prepared from healthy subjects were cultured in wells coated with a combination of OKT3 and anti-CD28 monoclonal antibody in the presence or absence of epinastine HCl for 24 h. The cells were also stimulated with interleukin (IL)-4 in a similar manner. Levels of TARC and IL-4 in culture supernatants were examined by ELISA. The addition of epinastine HCl exerted a dose-dependent suppressive effect on the production of both TARC and IL-4 from CD4+ T cells under co-stimulatory molecule stimulation. The minimum concentration of the agent showing a significant suppressive effect on TARC and IL-4 production was 5.0 microM and 2.5 microM, respectively. Epinastine HCl also suppressed the ability of cells to produce TARC in response to IL-4 stimulation, when the agent was added to cell cultures at more than 2.5 microM. It was concluded that this inhibitory action of epinastine HCl may be partially responsible for epinastine's attenuating effect on allergic diseases.
authors.affiliation: Department of Otolaryngology, School of Medicine, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.
authors.forename: Ken-Ichi
authors.initials: K
authors.lastname: Kanai
authors.forename: Kazuhito
authors.initials: K
authors.lastname: Asano
authors.forename: Tadashi
authors.initials: T
authors.lastname: Hisamitsu
authors.forename: Harumi
authors.initials: H
authors.lastname: Suzaki
mesh_terms: D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects* / Q000276:immunology; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D054414:Chemokine CCL17; D019742:Chemokines, CC / Q000037:antagonists & inhibitors* / Q000096:biosynthesis / Q000235:genetics; D003984:Dibenzazepines / Q000494:pharmacology*; D004306:Dose-Response Relationship, Immunologic; D006634:Histamine H1 Antagonists / Q000494:pharmacology*; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology*; D018189:Immunomagnetic Separation; D015847:Interleukin-4 / Q000037:antagonists & inhibitors / Q000276:immunology; D008213:Lymphocyte Activation / Q000187:drug effects; D008875:Middle Aged; D016853:Muromonab-CD3; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000187:drug effects* / Q000276:immunology
chemical_list: C106230:CCL17 protein, human; D054414:Chemokine CCL17; D019742:Chemokines, CC; D003984:Dibenzazepines; D006634:Histamine H1 Antagonists; D007093:Imidazoles; D016853:Muromonab-CD3; D016328:NF-kappa B; D015847:Interleukin-4; C053090:epinastine