The Effects of Lactobacillus rhamnosus on the Prevention of Asthma in a Murine Model.
10.4168/aair.2010.2.3.199
- Author:
Jinho YU
1
;
Seong Ok JANG
;
Byoung Ju KIM
;
Young Hwa SONG
;
Ji Won KWON
;
Mi Jin KANG
;
Won Ah CHOI
;
Hyun Don JUNG
;
Soo Jong HONG
Author Information
1. Department of Pediatrics, Childhood Asthma Atopy Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. sjhong@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
Asthma;
Lactobacillus rhamnosus;
probiotics;
primary prevention;
animal disease model
- MeSH:
Aged;
Animals;
Asthma;
Bacteria;
Bronchoalveolar Lavage;
Cell Count;
Disease Models, Animal;
Enzyme-Linked Immunosorbent Assay;
Eosinophils;
Gastroenteritis;
Humans;
Immunoglobulin E;
Immunoglobulin G;
Inflammation;
Lactobacillus;
Lactobacillus casei;
Lactobacillus rhamnosus;
Lung;
Methacholine Chloride;
Mice;
Ovalbumin;
Ovum;
Primary Prevention;
Probiotics
- From:Allergy, Asthma & Immunology Research
2010;2(3):199-205
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Lactobacilli are probiotic bacteria that are effective in the management of allergic diseases or gastroenteritis. It is hypothesized that such probiotics have immunoregulatory properties and promote mucosal tolerance. Our goal was to investigate whether Lactobacillus casei rhamnosus Lcr35 could inhibit airway inflammation in an ovalbumin (OVA)-induced murine model of asthma. METHODS: BALB/c mice aged 6 weeks were used in the present study. Lactobacillus casei rhamnosus Lcr35 was administered daily, starting 1 week prior to the first OVA sensitization (group 1) and 2 days before the first 1% OVA airway challenge (group 2). Mice that received only saline at both sensitization and airway challenge time points were used as negative controls (group 3), and those that had OVA-induced asthma were used as positive controls (group 4). Airway responsiveness to methacholine was assessed, and bronchoalveolar lavage (BAL) was performed. At the endpoint of the study, total IgE as well as OVA-specific IgE, IgG1 and IgG2a in serum was measured by enzyme-linked immunosorbent assay. Lung pathology was also evaluated. RESULTS: Airway hyperresponsiveness, total cell counts and the proportion of eosinophils in BAL fluid were significantly decreased in group 1 compared with group 4 (P<0.05). Total serum IgE levels were also significantly decreased in group 1 compared with group 4. Serum levels of OVA-specific IgE, IgG1 and IgG(2a) were not significantly influenced by treatment with Lcr35. There was significantly less peribronchial and perivascular infiltration of inflammatory cells in group 1 compared with group 4; however, there were no significant differences in methacholine challenge, BAL, serology or histology between groups 2 and 4. CONCLUSIONS: Oral treatment with Lcr35 prior to sensitization can attenuate airway inflammation and hyperreactivity in a mouse model of allergic airway inflammation. These results suggest that Lcr35 may have potential for preventing asthma.
