title: β-glucan curdlan induces IL-10-producing CD4+ T cells and inhibits allergic airway inflammation.
abstract: A number of studies have suggested a correlation between a decreased incidence in infectious diseases and an increased incidence of allergic diseases, including asthma. Although several pathogen-derived products have been shown to possess therapeutic potential for allergic diseases, it remains largely unknown whether β-glucan, a cell wall component of a variety of fungi, yeasts, and bacteria, has a regulatory potential for allergic diseases. In this study, we examined the effect of curdlan, a linear β-(1-3)-glucan, on the development of allergic airway inflammation. We found that i.p. injection of curdlan significantly inhibited Ag-induced eosinophil recruitment and Th2 cytokine production in the airways. The activation of CD4(+) T cells in the presence of curdlan induced IL-10-producing CD4(+) T cells with high levels of c-Maf expression. Curdlan-induced development of IL-10-producing CD4(+) T cells required the presence of APCs and ICOS/ICOS ligand interaction. Curdlan-induced development of IL-10-producing CD4(+) T cells also required intrinsic expression of STAT6. Furthermore, the transfer of Ag-specific CD4(+) T cells that were stimulated in the presence of curdlan inhibited Ag-induced eosinophil recruitment into the airways. Taken together, these results suggest that curdlan is capable of inducing IL-10-producing CD4(+) T cells and inhibiting the development of eosinohilic airway inflammation, underscoring the therapeutic potential of curdlan for allergic diseases.
authors.affiliation: Department of Allergy and Clinical Immunology, Graduate School of Medicine, Chiba University, Chiba 260-8670, Japan.
authors.forename: Saki
authors.initials: S
authors.lastname: Kawashima
authors.forename: Koichi
authors.initials: K
authors.lastname: Hirose
authors.forename: Arifumi
authors.initials: A
authors.lastname: Iwata
authors.forename: Kentaro
authors.initials: K
authors.lastname: Takahashi
authors.forename: Ayako
authors.initials: A
authors.lastname: Ohkubo
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Tamachi
authors.forename: Kei
authors.initials: K
authors.lastname: Ikeda
authors.forename: Shin-ichiro
authors.initials: S
authors.lastname: Kagami
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nakajima
mesh_terms: D000818:Animals; D016535:Bronchial Hyperreactivity / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism*; D002478:Cells, Cultured; D004802:Eosinophilia / Q000276:immunology / Q000473:pathology / Q000517:prevention & control; D018836:Inflammation Mediators / Q000008:administration & dosage* / Q000627:therapeutic use; D007274:Injections, Intraperitoneal; D016753:Interleukin-10 / Q000096:biosynthesis* / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D008822:Mice, Transgenic; D012130:Respiratory Hypersensitivity / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D047071:beta-Glucans / Q000008:administration & dosage* / Q000627:therapeutic use
chemical_list: C556062:IL10 protein, mouse; D018836:Inflammation Mediators; D047071:beta-Glucans; D016753:Interleukin-10; C038459:curdlan