Literature DB >> 25440975

Effects of immunomodulatory supplementation with Lactobacillus rhamnosus on airway inflammation in a mouse asthma model.

Chia-Ta Wu1, Peng-Jung Chen2, Yu-Tzu Lee3, Jiunn-Liang Ko3, Ko-Haung Lue4.   

Abstract

BACKGROUND: Asthma is a common allergic disease. In previous studies, probiotics improved the balance of intestinal microbes, reduced inflammation, and promoted mucosal tolerance. This study investigated whether oral administrations of Lactobacillus rhamnosus GG (LGG) inhibited allergen (ovalbumin or OVA)-induced airway inflammation in a mouse asthma model.
METHODS: The allergy/asthma animal model in this study was sensitization with OVA. After intranasal challenge with OVA, the airway inflammation and hyper-responsiveness were determined by a Buxco system, bronchoalveolar lavage fluid analysis with Liu stain, and enzyme-linked immunosorbent assay. Histopathologic changes in the lung were detected by hematoxylin and eosin staining and immunohistochemistry staining.
RESULTS: Both pre- and post-treatment with LGG suppressed the airway hyper-responsiveness to methacholine and significantly decreased the number of infiltrating inflammatory cells and Th2 cytokines in bronchoalveolar lavage fluid and serum compared with the OVA-sensitized mice. In addition, LGG reduced OVA-specific IgE levels in serum. Oral LGG decreased matrix metalloproteinase 9 expression in lung tissue and inhibited inflammatory cell infiltration.
CONCLUSION: LGG had an anti-inflammatory effect on OVA-induced airway inflammation and might be an additional or supplementary therapy for allergic airway diseases.
Copyright © 2014. Published by Elsevier B.V.

Entities:  

Keywords:  Lactobacillus rhamnosus GG; airway hyper-responsiveness; asthma; probiotics

Mesh:

Substances:

Year:  2014        PMID: 25440975     DOI: 10.1016/j.jmii.2014.08.001

Source DB:  PubMed          Journal:  J Microbiol Immunol Infect        ISSN: 1684-1182            Impact factor:   4.399


  28 in total

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10.  Preferential production of G-CSF by a protein-like Lactobacillus rhamnosus GR-1 secretory factor through activating TLR2-dependent signaling events without activation of JNKs.

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