title: Recombinant Lactobacillus plantarum inhibits house dust mite-specific T-cell responses.
abstract: Recent evidence suggests that chronic exposure to lactobacilli, which are part of the normal intestinal flora, inhibits the development of allergic disorders. Allergy is mediated by Th2 cells, which produce high levels of IL4 and IL5, and suppressive effects of lactic acid bacteria on the development of allergy have been attributed to their Th1-inducing properties. On the other hand, lactic acid bacteria have also been shown to suppress autoimmune disorders which are mediated by Th1 cells producing high levels of IFNgamma. To study this apparent discrepancy, the immunomodulatory potential of lactobacilli was evaluated using recombinants that express an immunodominant T-cell epitope of Der p 1 of house dust mites. Mucosal immunization of C57BL/6 J mice with such recombinants resulted in the induction of T cells which produced low amounts of IFNgamma. Immunization with the house dust mite peptide followed by treatment with recombinant Lactobacillus plantarum resulted in the inhibition of both IFNgamma and IL5 production. The effect on IFNgamma production was shown to be a non-specific effect of L. plantarum. The effect on IL5 production, however, was only observed when the recombinant expressing the Der p 1 peptide, but not the control recombinant, was used for treatment. Neither of the recombinants had an effect on the antibody response. Taken together, these data suggest that recombinant L. plantarum may be a suitable candidate for the treatment of allergic disorders.
authors.affiliation: Division of Immunological and Infectious Diseases, TNO-Prevention and Health, Leiden, The Netherlands.
authors.forename: A
authors.initials: A
authors.lastname: Kruisselbrink
authors.forename: M J
authors.initials: MJ
authors.lastname: Heijne Den Bak-Glashouwer
authors.forename: C E
authors.initials: CE
authors.lastname: Havenith
authors.forename: J E
authors.initials: JE
authors.lastname: Thole
authors.forename: R
authors.initials: R
authors.lastname: Janssen
mesh_terms: D000818:Animals; D039741:Antigens, Dermatophagoides; D002478:Cells, Cultured; D004391:Dust / Q000009:adverse effects; D005260:Female; D006023:Glycoproteins / Q000235:genetics / Q000276:immunology; D006969:Hypersensitivity, Immediate / Q000276:immunology*; D007073:Immunoglobulin E / Q000096:biosynthesis; D007074:Immunoglobulin G / Q000096:biosynthesis; D007371:Interferon-gamma / Q000096:biosynthesis; D015848:Interleukin-5 / Q000096:biosynthesis; D007778:Lactobacillus / Q000235:genetics* / Q000378:metabolism / Q000502:physiology*; D008213:Lymphocyte Activation; D051379:Mice; D008810:Mice, Inbred C57BL; D008925:Mites / Q000276:immunology*; D011993:Recombinant Fusion Proteins / Q000276:immunology / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology; D014169:Transformation, Bacterial
chemical_list: D039741:Antigens, Dermatophagoides; D004391:Dust; D006023:Glycoproteins; D007074:Immunoglobulin G; D015848:Interleukin-5; D011993:Recombinant Fusion Proteins; D007073:Immunoglobulin E; D007371:Interferon-gamma