title: Oral administration of Lactobacillus delbrueckii subspecies bulgaricus OLL1073R-1 suppresses inflammation by decreasing interleukin-6 responses in a murine model of atopic dermatitis.
abstract: The oral intake of Lactobacillus spp. can provide beneficial effects to the host by modulating the immune response. Atopic dermatitis (AD) is an allergic inflammatory disease mediated by various immune responses. In this study, we examined the effect of a Lactobacillus strain, Lactobacillus delbrueckii ssp. bulgaricus OLL1073R-1 (OLL1073R-1), on AD development in a murine model of AD that was developed by the topical application of mite antigen in NC/Nga mice. The oral intake of heat-killed OLL1073R-1 cells inhibited both the development of dermatitis and the elevation of an acute inflammation marker, serum amyloid A. Another bacterial strain, Lactobacillus rhamnosus OLL2984, exerted no inhibitory effects on dermatitis. The oral intake of heat-killed OLL1073R-1 cells also attenuated secretion of IL-6 from lymph node cells in response to mite antigen and reduced IL-6 levels in inflamed tissues, such as auricles. Production of IFN-γ or IL-4 was not influenced by OLL1073R-1 intake. We also found that inhibition of IL-6 signaling by gp130-Fc (a fusion protein consisting of the extracellular portion of glycoprotein 130 fused to the Fc region of human IgG1) markedly decreased the severity of dermatitis in NC/Nga mice. Moreover, secretion of IL-6 by lymph node cells was augmented in NC/Nga mice compared with that in BALB/c mice. These results indicate that IL-6 plays an essential role in the development of dermatitis in the NC/Nga mouse model of AD, and that OLL1073R-1 inhibits dermatitis, at least in part, by suppressing the IL-6 response.
authors.affiliation: Food Science Research Laboratories, Meiji Corporation, 540 Naruda, Odawara, Kanagawa 250-0862, Japan. hiroshi.kano@meiji.com
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kano
authors.forename: Junko
authors.initials: J
authors.lastname: Kita
authors.forename: Seiya
authors.initials: S
authors.lastname: Makino
authors.forename: Shuji
authors.initials: S
authors.lastname: Ikegami
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Itoh
mesh_terms: D000818:Animals; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000517:prevention & control* / Q000628:therapy; D004195:Disease Models, Animal; D005260:Female; D006023:Glycoproteins / Q000008:administration & dosage / Q000235:genetics; D007073:Immunoglobulin E / Q000097:blood; D007141:Immunoglobulin Fc Fragments / Q000008:administration & dosage / Q000235:genetics; D007074:Immunoglobulin G / Q000008:administration & dosage / Q000235:genetics; D007249:Inflammation / Q000517:prevention & control*; D015850:Interleukin-6 / Q000502:physiology*; D048668:Lactobacillus delbrueckii / Q000276:immunology* / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D011993:Recombinant Fusion Proteins / Q000008:administration & dosage; D015398:Signal Transduction / Q000187:drug effects; D013047:Specific Pathogen-Free Organisms
chemical_list: D006023:Glycoproteins; D007141:Immunoglobulin Fc Fragments; D007074:Immunoglobulin G; D015850:Interleukin-6; D011993:Recombinant Fusion Proteins; C480482:glycoprotein 130, human; D007073:Immunoglobulin E