title: Bifidobacterium breve and Streptococcus thermophilus secretion products enhance T helper 1 immune response and intestinal barrier in mice.
abstract: Lactic acid bacteria or their secretion products can modulate immune responses differently in normal and inflammatory conditions. This comparative study analyzes the effect of oral administration of living lactic acid bacteria, or their conditioned media, on the epithelial and immune functions of colitis-prone C57BL/6 IL-10-deficient mice. Mice were untreated (control) or infected with Helicobacter hepaticus with or without oral treatment with living bacteria, Bifidobacterium breve C50 and Streptococcus thermophilus 065 (LB), or their culture-conditioned media (CM). Histology, cytokine mRNA, electrical resistance, and barrier capacity of colonic samples as well as cytokine secretion by mesenteric lymph node (MLN) cells were studied. Helicobacter hepaticus mice developed only mild colitis, which was not modified in LB or CM groups. In the CM (but not the LB) group, the colonic barrier was reinforced as compared to the other groups, as evidenced by decreased horseradish peroxidase (HRP) transcytosis and mannitol fluxes and increased electrical resistance. In MLN, the percentage of CD4+ and CD8+ T cells secreting IFNgamma was significantly higher in CM (2.06% and 1.98%, respectively) mice than in H. hepaticus (1.1% and 0.47%, P < 0.05) or control mice. In addition, the nonspecific stimulation of IFNgamma, TNFalpha, and IL-12 secretion by MLN cells was significantly higher in the CM group as compared to the other groups. In the absence of severe colitis, Bifidobacterium breve C50- and Streptococcus thermophilus 065-conditioned media can reinforce intestinal barrier capacity and stimulate Th1 immune response, highlighting the involvement of lactic acid bacteria-derived components in host defense.
authors.affiliation: INSERM EMI 0212, Faculté Cochin Necker, 156 rue de Vaugirard, 75730 Paris, France.
authors.forename: Sandrine
authors.initials: S
authors.lastname: Ménard
authors.forename: David
authors.initials: D
authors.lastname: Laharie
authors.forename: Corinne
authors.initials: C
authors.lastname: Asensio
authors.forename: Teresita
authors.initials: T
authors.lastname: Vidal-Martinez
authors.forename: Céline
authors.initials: C
authors.lastname: Candalh
authors.forename: Anne
authors.initials: A
authors.lastname: Rullier
authors.forename: Frank
authors.initials: F
authors.lastname: Zerbib
authors.forename: Francis
authors.initials: F
authors.lastname: Mégraud
authors.forename: Tamara
authors.initials: T
authors.lastname: Matysiak-Budnik
authors.forename: Martine
authors.initials: M
authors.lastname: Heyman
mesh_terms: D000818:Animals; D001644:Bifidobacterium / Q000378:metabolism*; D002478:Cells, Cultured; D016207:Cytokines / Q000032:analysis / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D004926:Escherichia coli / Q000276:immunology; D004927:Escherichia coli Infections / Q000276:immunology / Q000473:pathology; D005260:Female; D005434:Flow Cytometry; D016481:Helicobacter Infections / Q000276:immunology / Q000473:pathology; D044923:Helicobacter hepaticus / Q000276:immunology; D007413:Intestinal Mucosa / Q000276:immunology*; D007422:Intestines / Q000166:cytology / Q000276:immunology; D008198:Lymph Nodes / Q000166:cytology; D051379:Mice; D008810:Mice, Inbred C57BL; D020133:Reverse Transcriptase Polymerase Chain Reaction; D048249:Streptococcus thermophilus / Q000378:metabolism*; D018417:Th1 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines