Roflumilast reduces allergen-induced airway inflammation in patients with asthma – Healio

Roflumilast reduces allergen-induced airway inflammation in patients with asthma
Healio
“The studies presented here show that roflumilast has no acute bronchodilator actions in patients with mild to moderate asthma,” Philip Bardin, PhD, the director of the lung and sleep unit at Monash Health in Australia, and colleagues wrote. “This

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STAT1 Attenuates Murine Allergen-Induced Airway Remodeling and Exacerbation by Carbon Nanotubes.

STAT1 Attenuates Murine Allergen-Induced Airway Remodeling and Exacerbation by Carbon Nanotubes.

Am J Respir Cell Mol Biol. 2015 Mar 25;

Authors: Thompson EA, Sayers BC, Glista-Baker EE, Shipkowski KA, Ihrie MD, Duke KS, Taylor AJ, Bonner JC

Abstract
Asthma is characterized by a T-helper 2 (Th2) phenotype and by chronic allergen-induced airway inflammation (AAI). Environmental exposure to air pollution ultrafine particles (i.e., nanoparticles) exacerbates AAI and a concern is possible exacerbation posed by engineered nanoparticles generated by emerging nanotechnologies. STAT1 is a transcription factor that maintains Th1 cell development. However, the role of STAT1 in regulating AAI or exacerbation by nanoparticles has not been explored. In this study, mice with whole body knock-out of the Stat1 gene (Stat1-/-) or wild type (WT) mice were sensitized to ovalbumin (OVA) allergen and then exposed to multi-walled carbon nanotubes (MWCNTs) by oropharygneal aspiration. In Stat1-/- and WT mice, OVA increased eosinophils in bronchoalveolar lavage fluid (BALF), while MWCNTs increased neutrophils. Interestingly, OVA sensitization prevented MWCNT-induced neutrophilia and caused only eosinophilic inflammation. Stat1-/- mice displayed increased IL-13 in BALF 1 day compared to WT mice after treatment with OVA or OVA and MWCNT. At 21 days the lungs of OVA-sensitized Stat1-/- mice displayed increased eosinophilia, goblet cell hyperplasia, airway fibrosis, and subepithelial apoptosis. MWCNTs further increased OVA-induced goblet cell hyperplasia, airway fibrosis, and apoptosis in Stat1-/- mice at 21 days. These changes corresponded to increased levels of pro-fibrogenic mediators (TGF-?1, TNF-?, OPN) but decreased IL-10 in Stat1-/- mice. Finally, fibroblasts isolated from the lungs of Stat1-/- mice produced significantly more collagen mRNA and protein in response to TGF-?1 compared to WT lung fibroblasts. Our results support a protective role for STAT1 in chronic AAI and exacerbation of remodeling caused by MWCNTs.

PMID: 25807359 [PubMed – as supplied by publisher]

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Researchers discover molecule that could treat allergen-induced asthma – Medical News Today


UPI.com

Researchers discover molecule that could treat allergen-induced asthma
Medical News Today
Asthma affects more than 25 million people in the US, with around 60% of these cases resulting from allergies. Now, researchers have discovered a molecule that they say could prevent symptoms triggered by allergen-induced asthma. The research team …
Synthetic molecule thwarts asthma symptomsUPI.com
Researchers Discover Novel Molecule to Treat AsthmaDrug Discovery & Development
Novel Molecule Offers Hope for Asthma SufferersGenetic Engineering News
Design & Trend
all 25 news articles »

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Reduce Inflammation in Allergen-Induced Asthma by Herbal Medicine Treatment – AccentedTouch


AccentedTouch

Reduce Inflammation in Allergen-Induced Asthma by Herbal Medicine Treatment
AccentedTouch
Researchers have found that a traditional Korean medicine that has protracted been used for the treatment of allergic diseases in Asia can lessen inflammation in allergen-induced asthma. “Researchers from Boston University School of Medicine (BUSM),

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Herbal medicine treatment reduces inflammation in allergen-induced asthma … – Science Daily (press release)

Herbal medicine treatment reduces inflammation in allergen-induced asthma
Science Daily (press release)
These findings appear online in the Annals of Allergy, Asthma & Immunology. Asthma is a unique form of chronic respiratory disease characterized by reversible airway obstruction and pulmonary inflammation. It represents one of the most common chronic

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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.

Related Articles

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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