Bronchial lesions of mouse model of asthma are preceded by immune complex vasculitis and induced bronchial associated lymphoid tissue (iBALT).

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Bronchial lesions of mouse model of asthma are preceded by immune complex vasculitis and induced bronchial associated lymphoid tissue (iBALT).

Lab Invest. 2015 Jun 1;

Authors: Guest IC, Sell S

Abstract
We systematically examined by immune histology the lungs of some widely used mouse models of asthma. These models include sensitization by multiple intraperitoneal injections of soluble ovalbumin (OVA) or of OVA with alum, followed by three intranasal or aerosol challenges 3 days apart. Within 24?h after a single challenge there is fibrinoid necrosis of arterial walls with deposition of immunoglobulin (Ig) and OVA and infiltration of eosinophilic polymorphonuclear cells that lasts for about 3 days followed by peribronchial B-cell infiltration and slight reversible goblet cell hypertrophy (GCHT). After two challenges, severe eosinophilic vasculitis is present at 6?h, increases by 72?h, and then declines; B-cell proliferation and significant GCHT and hyperplasia (GCHTH) and bronchial smooth muscle hypertrophy recur more prominently. After three challenges, there is significantly increased induced bronchus-associated lymphoid tissue (iBALT) formation, GCHTH, and smooth muscle hypertrophy. Elevated levels of Th2 cytokines, IL-4, IL-5, and IL-13, are present in bronchial lavage fluids. Sensitized mice have precipitating antibody and positive Arthus skin reactions but also develop significant levels of IgE antibody to OVA but only 1 week after challenge. We conclude that the asthma like lung lesions induced in these models is preceded by immune complex-mediated eosinophilic vasculitis and iBALT formation. There are elevations of Th2 cytokines that most likely produce bronchial lesions that resemble human asthma. However, it is unlikely that mast cell-activated atopic mechanisms are responsible as we found only a few presumed mast cells by toluidine blue and metachromatic staining limited to the most proximal part of the main stem bronchus, and none in the remaining main stem bronchus or in the lung periphery.Laboratory Investigation advance online publication, 1 June 2015; doi:10.1038/labinvest.2015.72.

PMID: 26006019 [PubMed – as supplied by publisher]

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Bronchial lesions of mouse model of asthma are preceded by immune complex … – Nature.com

Bronchial lesions of mouse model of asthma are preceded by immune complex
Nature.com
We systematically examined by immune histology the lungs of some widely used mouse models of asthma. These models include sensitization by multiple intraperitoneal injections of soluble ovalbumin (OVA) or of OVA with alum, followed by three intranasal …

View full post on asthma – Google News

Budesonide comparable to methylprednisolone for pediatric bronchial asthma … – Healio

Budesonide comparable to methylprednisolone for pediatric bronchial asthma
Healio
Methylprednisolone and budesonide inhalation suspension showed limited differences regarding the severity of attacks, duration of management, duration of wheezing and hospitalization in patients with moderate bronchial asthma attacks, according to

and more »

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Insurers reluctant to cover pricey bronchial thermoplasty asthma treatment – FierceHealthPayer


FierceHealthPayer

Insurers reluctant to cover pricey bronchial thermoplasty asthma treatment
FierceHealthPayer
BCBS changed its policy based on bronchial thermoplasty studies and noted that only a small subset of individuals with severe asthma meet the criteria, which includes demonstrating that previous asthma drug treatments didn't work, HCSC spokeswoman …

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Undifferentiated Bronchial Fibroblasts Derived from Asthmatic Patients Display Higher Elastic Modulus than Their Non-Asthmatic Counterparts.

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Undifferentiated Bronchial Fibroblasts Derived from Asthmatic Patients Display Higher Elastic Modulus than Their Non-Asthmatic Counterparts.

PLoS One. 2015;10(2):e0116840

Authors: Sarna M, Wojcik KA, Hermanowicz P, Wnuk D, Burda K, Sanak M, Czy? J, Michalik M

Abstract
During asthma development, differentiation of epithelial cells and fibroblasts towards the contractile phenotype is associated with bronchial wall remodeling and airway constriction. Pathological fibroblast-to-myofibroblast transition (FMT) can be triggered by local inflammation of bronchial walls. Recently, we have demonstrated that human bronchial fibroblasts (HBFs) derived from asthmatic patients display some inherent features which facilitate their FMT in vitro. In spite of intensive research efforts, these properties remain unknown. Importantly, the role of undifferentiated HBFs in the asthmatic process was systematically omitted. Specifically, biomechanical properties of undifferentiated HBFs have not been considered in either FMT or airway remodeling in vivo. Here, we combine atomic force spectroscopy with fluorescence microscopy to compare mechanical properties and actin cytoskeleton architecture of HBFs derived from asthmatic patients and non-asthmatic donors. Our results demonstrate that asthmatic HBFs form thick and aligned ‘ventral’ stress fibers accompanied by enlarged focal adhesions. The differences in cytoskeleton architecture between asthmatic and non-asthmatic cells correlate with higher elastic modulus of asthmatic HBFs and their increased predilection to TGF-?-induced FMT. Due to the obvious links between cytoskeleton architecture and mechanical equilibrium, our observations indicate that HBFs derived from asthmatic bronchi can develop considerably higher static tension than non-asthmatic HBFs. This previously unexplored property of asthmatic HBFs may be potentially important for their myofibroblastic differentiation and bronchial wall remodeling during asthma development.

PMID: 25679502 [PubMed – as supplied by publisher]

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Bronchial thermoplasty for severe asthma: an interview with Dr. Rob Niven – News-Medical.net

Bronchial thermoplasty for severe asthma: an interview with Dr. Rob Niven
News-Medical.net
Internationally, severe asthma is defined as anybody who is on maximum therapy, which has no measurable side effects, but still have symptoms of persistent asthma. In the UK, that effectively means people who require oral steroids for their asthma two

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