Probiotic-induced suppression of allergic sensitization and airway inflammation is associated with an increase of T regulatory-dependent mechanisms in a murine model of asthma

Clin Exp Allergy. 2007 Apr;37(4):498-505. doi: 10.1111/j.1365-2222.2006.02629.x.


Background: Microbial intestinal colonization in early in life is regarded to play a major role for the maturation of the immune system. Application of non-pathogenic probiotic bacteria during early infancy might protect from allergic disorders but underlying mechanisms have not been analysed so far.

Objective: The aim of the current study was to investigate the immune effects of oral application of probiotic bacteria on allergen-induced sensitization and development of airway inflammation and airway hyper-reactivity, cardinal features of bronchial asthma.

Methods: Newborn Balb/c mice received orally 10(9) CFU every second day either Lactobacillus rhamnosus GG or Bifidobacterium lactis (Bb-12) starting from birth for consecutive 8 weeks, during systemic sensitization (six intraperitoneal injections, days 29-40) and airway challenge (days 54-56) with ovalbumin.

Results: The administration of either Bb-12 or LGG suppressed all aspects of the asthmatic phenotype: airway reactivity, antigen-specific immunoglobulin E production and pulmonary eosinophilia (mean: 137 vs. 17 and 13 cellsx10(3)/mL, respectively). Antigen-specific recall proliferation by spleen cells and T-helper type 2 cytokine production (IL-4, IL-5 and IL-10) by mesenteric lymph node cells also showed significant reduction, while TGF production remained unchanged. Oral LGG administration particularly suppressed allergen-induced proliferative responses and was associated with an increase in numbers of TGF-beta-secreting CD4+/CD3+ T cells in mesenteric lymph nodes (6.5, 16.7%) as well as nearly 2-fold up-regulation of Foxp3-expressing cells in peribronchial lymph nodes.

Conclusions: Neonatal application of probiotic bacteria inhibits subsequent allergic sensitization and airway disease in a murine model of asthma by induction of T regulatory cells associated with increased TGF-beta production.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Allergens / immunology
  • Animals
  • Asthma / immunology
  • Asthma / physiopathology
  • Asthma / prevention & control*
  • Bifidobacterium / immunology
  • Bronchial Hyperreactivity / immunology
  • Bronchial Hyperreactivity / prevention & control
  • Cell Proliferation
  • Cytokines / biosynthesis
  • Disease Models, Animal
  • Eosinophilia / prevention & control
  • Female
  • Forkhead Transcription Factors / metabolism
  • Immunoglobulin E / biosynthesis
  • Immunoglobulin G / biosynthesis
  • Lacticaseibacillus rhamnosus / immunology
  • Lymph Nodes / immunology
  • Mice
  • Mice, Inbred BALB C
  • Ovalbumin / immunology
  • Probiotics / therapeutic use*
  • Reverse Transcriptase Polymerase Chain Reaction / methods
  • Spleen / immunology
  • T-Lymphocytes, Regulatory / immunology*
  • Transforming Growth Factor beta / metabolism
  • Up-Regulation / immunology


  • Allergens
  • Cytokines
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • Immunoglobulin G
  • Transforming Growth Factor beta
  • Immunoglobulin E
  • Ovalbumin