Asthma Prevention by Lactobacillus Rhamnosus in a Mouse Model is Associated With CD4(+)CD25(+)Foxp3(+) T Cells.

Asthma Prevention by Lactobacillus Rhamnosus in a Mouse Model is Associated With CD4(+)CD25(+)Foxp3(+) T Cells.

Allergy Asthma Immunol Res. 2012 May;4(3):150-6

Authors: Jang SO, Kim HJ, Kim YJ, Kang MJ, Kwon JW, Seo JH, Kim HY, Kim BJ, Yu J, Hong SJ

Abstract
PURPOSE: Probiotic bacteria can induce immune regulation or immune tolerance in allergic diseases. The underlying mechanisms have been recently investigated, but are still unclear. The aim of this study was to evaluate the protective effects of the probiotic Lactobacillus rhamnosus (Lcr35) in a mouse model of asthma and to identify its mechanism of action.
METHODS: Lcr35 was administered daily by the oral route at a dosage of 1×10(9) CFU/mouse in BALB/c mice for 7 days before the first sensitization. Clinical parameters and regulatory T (Treg) cells were examined. The role of CD4(+)CD25(+)Foxp3(+) Treg cells was analyzed using a Treg cell-depleting anti-CD25 monoclonal antibody (mAb).
RESULTS: Airway hyperresponsiveness, total IgE production, pulmonary eosinophilic inflammation, and splenic lymphocyte proliferation were suppressed after Lcr35 treatment. Th1 (IFN-?) and Th2 (IL-4, IL-5, and IL-13) cytokines in the serum were suppressed, and the percentage of CD4(+)CD25(+)Foxp3(+) Treg cells in the spleen was significantly increased in the Lcr35 treatment group. Anti-CD25 mAb administration abolished the protective effects of Lcr35, indicating that CD4(+) CD25(+)Foxp3(+) Treg cells are essential in mediating the activity of Lcr35.
CONCLUSIONS: Oral administration of Lcr35 attenuated the features of allergic asthma in a mouse model and induced immune regulation by a CD4(+)CD25(+)Foxp3(+) Treg cell-mediated mechanism.

PMID: 22548208 [PubMed – in process]

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Antibiotics linked to asthma in mouse study – CBC.ca


CBC.ca

Antibiotics linked to asthma in mouse study
CBC.ca
A new study conducted on mice suggests that antibiotics taken in childhood could play a part in the development and severity of allergic asthma. The study published Friday in the journal EMBO reports that antibiotics may damage bacteria that live in
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Asthma, gamma-interferon, and the mouse that didn’t wheeze – Scope (blog)


Scope (blog)

Asthma, gamma-interferon, and the mouse that didn't wheeze
Scope (blog)
In a just-out study, Stanford's Steve Galli, MD, Mang Yu, MD, PhD, and their colleagues induced a condition very closely mimicking asthma's molecular and cellular symptoms, not just the wheezing, in lab mice. But doing so required the active
Key immune substance linked to asthma, Stanford study findsEurekAlert (press release)

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Cigarette smoke exacerbates mouse allergic asthma through Smad proteins … – 7thSpace Interactive (press release)

Cigarette smoke exacerbates mouse allergic asthma through Smad proteins
7thSpace Interactive (press release)
Many studies have found that smoking reduces lung function, but the relationship between cigarette smoke and allergic asthma has not been clearly elucidated, particularly the role of mast cells. This study aimed to investigate the effects of smoke

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Allergen-Induced Coexpression of bFGF and TGF-?1 by Macrophages in a Mouse Model of Airway Remodeling: bFGF Induces Macrophage TGF-?1 Expression in vitro.

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Allergen-Induced Coexpression of bFGF and TGF-?1 by Macrophages in a Mouse Model of Airway Remodeling: bFGF Induces Macrophage TGF-?1 Expression in vitro.

Int Arch Allergy Immunol. 2010 Nov 25;155(1):12-22

Authors: Yum HY, Cho JY, Miller M, Broide DH

Background: Basic fibroblast growth factor (bFGF) is a cytokine that is mitogenic for fibroblasts and smooth muscle and may play a role in airway remodeling in asthma. We have used a mouse model of chronic ovalbumin (OVA) allergen-induced airway remodeling to determine whether bFGF and fibroblast growth factor receptor-1 are expressed and regulated by corticosteroids in the airway, as well as to determine whether bFGF mediates expression of another proremodeling cytokine, transforming growth factor (TGF)-?1. Methods: The airway levels and localization of bFGF, FGF receptor-1 and TGF-?1 were determined by ELISA, immunohistology and image analysis in the remodeled airways of chronic OVA-challenged mice treated with either corticosteroids or diluent. In vitro cultures of bone narrow-derived macrophages were used to determine whether bFGF induced TGF-?1 expression. Results: Mice chronically challenged with OVA developed significant airway remodeling that was associated with significantly increased levels of bFGF and TGF-?1. Immunohistochemistry demonstrated significantly increased bFGF and FGF receptor-1 expression by peri- bronchial F4/80+ cells. Double-label immunofluorescence microscopy studies demonstrated that peribronchial macrophages coexpressed bFGF and TGF-?1. In vitro studies demonstrated that incubation of bone marrow-derived macrophages with bFGF induced expression of TGF-?1. Mice treated with corticosteroids and subjected to chronic OVA challenge had significantly reduced levels of bFGF, FGF receptor-1, peribronchial TGF-?1+ cells and airway remodeling. Conclusions: Overall, this study demonstrates that allergen challenge stimulates peribronchial macrophages to coexpress bFGF and TGF-?1 and that bFGF may potentiate macrophage release of TGF-?1 through autocrine and/or paracrine pathways.

PMID: 21109744 [PubMed – as supplied by publisher]

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Protective Effects of Mentha haplocalyx Ethanol Extract (MH) in a Mouse Model of Allergic Asthma.

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Protective Effects of Mentha haplocalyx Ethanol Extract (MH) in a Mouse Model of Allergic Asthma.

Phytother Res. 2010 Nov 24;

Authors: Lee MY, Lee JA, Seo CS, Ha H, Lee NH, Shin HK

Mentha haplocalyx Briq., a commonly used herb in traditional Oriental medicine, has a variety of known pharmacological properties. However, neither the protective effects of Mentha haplocalyx ethanol extract (MH) against inflammation of the airway in an asthmatic model nor the mechanisms involved, have previously been reported. In the present study, an ovalbumin (OVA)-induced mouse model of allergic asthma was used to investigate whether MH was effective against the disease through regulation of airway inflammation. The MH treatment significantly inhibited increases in immunoglobulin (Ig) E and T-helper 2 (Th2)-type cytokines such as IL-4 and IL-5 in bronchoalveolar lavage fluid (BALF) and lung tissue. Inflammatory cell infiltration of the airway in mice treated with MH was effectively alleviated when compared with infiltration seen in the OVA-induced group. These data indicated that decreased cytokine levels are the result of the decreased number of invaded leukocytes. Also, the generation of reactive oxygen species (ROS) in BALF was diminished by MH treatment. Taken together, these findings indicate that the administration of MH may have potential therapeutic value in the treatment of inflammatory disease. Copyright © 2010 John Wiley & Sons, Ltd.

PMID: 21108485 [PubMed – as supplied by publisher]

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Treatment for S. aureus skin infection works in mouse model

Scientists from the National Institutes of Health and University of Chicago have found a promising treatment method that in laboratory mice reduces the severity of skin and soft-tissue damage caused by USA300, the leading cause of community-associated Staphylococcus aureus infections in the United States. By neutralizing a key toxin associated with the bacteria, they found they could greatly reduce the damaging effects of the infection on skin and soft tissue. Community strains of S. aureus cause infection in otherwise healthy people and are considered extremely virulent, as opposed to hospital strains that infect people who already are weakened by illness or surgery.

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Systemic lupus erythematosus: From mouse models to human disease and treatment

On Sept. 2-3, 2010, the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), the National Cancer Institute (NCI), the National Institute of Allergy and Infectious Diseases (NIAID), and the NIH Office of Research on Women’s Health (ORWH) will convene a two-day conference on Systemic Lupus Erythematosus: From Mouse Models to Human Disease and Treatment. This meeting will bring together basic research scientists working on models of autoimmune disease relevant to systemic lupus erythematosus (SLE), with clinicians treating lupus patients. There are numerous mouse models of lupus, but their relevance to the actual disorder is still a subject for debate. Moreover, since SLE is a heterogeneous disease, some features of the disorder may be better reflected in one or another mouse model.

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