• Media type: E-Article
  • Title: Longitudinal study of effects of oral dosage of Bifidobacterium bifidum G9‐1 on Japanese cedar pollen‐induced allergic nasal symptoms in guinea pigs
  • Contributor: Tsunemine, Satoru; Isa, Yasuhiro; Ohno, Hiroshi; Hagino, Satoko; Yamamura, Hideki; Mizutani, Nobuaki; Nabe, Takeshi
  • Published: Wiley, 2015
  • Published in: Microbiology and Immunology, 59 (2015) 11, Seite 690-699
  • Language: English
  • DOI: 10.1111/1348-0421.12324
  • ISSN: 0385-5600; 1348-0421
  • Origination:
  • Footnote:
  • Description: ABSTRACTPrevious studies using experimental animal models have reported the beneficial effects of probiotics on allergic responses; however, their long‐term effects on allergic nasal symptoms in clinical settings have not yet been elucidated in detail. In the present study, a guinea pig allergic rhinitis model involving repeated inhalation challenges with a natural allergen, Japanese cedar pollen, was used to examine the longitudinal effects of Bifidobacterium bifidum G9‐1 (BBG9‐1) on allergic nasal symptoms. BBG9‐1 was administered orally once a day. Amelioration of nasal blockage was consistently observed throughout the experimental period in the BBG9‐1‐treated group. Although challenge‐induced sneezing was not significantly inhibited in the BBG9‐1‐treated group, prolonged treatment with BBG9‐1 slightly reduced the frequency of sneezing. Antigen‐specific IgE antibody production was also not inhibited in the BBG9‐1‐treated group. Increases in the numbers of eosinophils and neutrophils in nasal cavity lavage fluid collected after pollen challenge were almost completely suppressed by BBG9‐1 treatment, whereas those in mast cell mediators, histamine and cysteinyl leukotrienes were not. In contrast, increases in the levels of nitric oxide metabolites were potently suppressed. Furthermore, prolonged BBG9‐1 treatment markedly suppressed exogenous leukotriene D4‐induced nasal blockage. Thus, prolonged oral administration of BBG9‐1 suppresses Japanese cedar pollen‐induced allergic nasal symptoms. The inhibitory mechanisms responsible may involve reductions in the responsiveness of target organs, such as endothelial cells in nasal mucosal blood vessels, to chemical mediators.
  • Access State: Open Access