title: Oral treatment with live Lactobacillus reuteri inhibits the allergic airway response in mice.
abstract: BACKGROUND
  Clinical trials have demonstrated that probiotics may be effective in the treatment and prevention of atopic disease in children but there have been few reports of therapeutic effects of oral probiotics outside the gastrointestinal tract.
  
  
  OBJECTIVE
  We investigated the effect of two probiotic organisms on the response to antigen challenge in a mouse model of allergic airway inflammation.
  
  
  METHODS
  We used an ovalbumin-sensitized asthma model in BALB/c and Toll-like receptor 9-deficient mice. Animals were treated with probiotic organisms via gavaging needle before antigen challenge. After antigen challenge, airway responsiveness to methacholine, influx of inflammatory cells to the lung, and cytokine levels in bronchoalveolar lavage fluid were assessed.
  
  
  RESULTS
  Oral treatment with live Lactobacillus reuteri but not Lactobacillus salivarius significantly attenuated the influx of eosinophils to the airway lumen and parenchyma and reduced the levels of tumor necrosis factor, monocyte chemoattractant protein-1, IL-5, and IL-13 in bronchoalveolar lavage fluid of antigen-challenged animals, but there was no change in eotaxin or IL-10. L. reuteri but not L. salivarius also decreased allergen-induced airway hyperresponsiveness. These responses were dependent on Toll-like receptor 9 and were associated with increased activity of indoleamine 2,3-dioxygenase. Killed organisms did not mimic the ability of the live L. reuteri to attenuate inflammation or airway hyperresponsiveness.
  
  
  CONCLUSIONS
  Oral treatment with live L. reuteri can attenuate major characteristics of an asthmatic response in a mouse model of allergic airway inflammation. These results suggest that oral treatment with specific live probiotic strains may have therapeutic potential in the treatment of allergic airway disease.
authors.affiliation: Department of Pathology, Brain-Body Institute, Hamilton, ON, L8N 4A6 Canada.
authors.forename: Paul
authors.initials: P
authors.lastname: Forsythe
authors.forename: Mark D
authors.initials: MD
authors.lastname: Inman
authors.forename: John
authors.initials: J
authors.lastname: Bienenstock
mesh_terms: D000284:Administration, Oral; D000818:Animals; D001249:Asthma / Q000628:therapy*; D016535:Bronchial Hyperreactivity / Q000628:therapy*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D016085:Bronchoconstrictor Agents / Q000494:pharmacology; D016207:Cytokines / Q000378:metabolism; D004269:DNA, Bacterial / Q000302:isolation & purification; D004195:Disease Models, Animal; D004804:Eosinophils / Q000378:metabolism; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase / Q000097:blood; D007737:Kynurenine / Q000097:blood; D052200:Limosilactobacillus reuteri; D008297:Male; D016210:Methacholine Chloride / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D019936:Probiotics / Q000008:administration & dosage*; D051217:Toll-Like Receptor 9; D014364:Tryptophan / Q000097:blood
chemical_list: D016085:Bronchoconstrictor Agents; D016207:Cytokines; D004269:DNA, Bacterial; D050503:Indoleamine-Pyrrole 2,3,-Dioxygenase; D051217:Toll-Like Receptor 9; D016210:Methacholine Chloride; D007737:Kynurenine; D014364:Tryptophan