Research team learns more about why airway closes up during asthma attacks – Medical Xpress


Medical Xpress

Research team learns more about why airway closes up during asthma attacks
Medical Xpress
The molecular regulation of smooth-muscle contraction is an important determinant of airway responses during an acute asthmatic attack. In acute asthma, various triggers, including viral illnesses and aeroallergens, can cause acute narrowing of the

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UCSF Team Learns More About Why Airway Closes Up During Asthma Attacks – UCSF News Services


UCSF News Services

UCSF Team Learns More About Why Airway Closes Up During Asthma Attacks
UCSF News Services
The molecular regulation of smooth-muscle contraction is an important determinant of airway responses during an acute asthmatic attack. In acute asthma, various triggers, including viral illnesses and aeroallergens, can cause acute narrowing of the

View full post on asthma – Google News

Lung-Homing of Endothelial Progenitor Cells and Airway Vascularization Is Only Partially Dependant on Eosinophils in a House Dust Mite-Exposed Mouse Model of Allergic Asthma.

Related Articles

Lung-Homing of Endothelial Progenitor Cells and Airway Vascularization Is Only Partially Dependant on Eosinophils in a House Dust Mite-Exposed Mouse Model of Allergic Asthma.

PLoS One. 2014;9(10):e109991

Authors: Sivapalan N, Wattie J, Inman MD, Sehmi R

Abstract
BACKGROUND: Asthmatic responses involve a systemic component where activation of the bone marrow leads to mobilization and lung-homing of progenitor cells. This traffic may be driven by stromal cell derived factor-1 (SDF-1), a potent progenitor chemoattractant. We have previously shown that airway angiogenesis, an early remodeling event, can be inhibited by preventing the migration of endothelial progenitor cells (EPC) to the lungs. Given intranasally, AMD3100, a CXCR4 antagonist that inhibits SDF-1 mediated effects, attenuated allergen-induced lung-homing of EPC, vascularization of pulmonary tissue, airway eosinophilia and development of airway hyperresponsiveness. Since SDF-1 is also an eosinophil chemoattractant, we investigated, using a transgenic eosinophil deficient mouse strain (PHIL) whether EPC lung accumulation and lung vascularization in allergic airway responses is dependent on eosinophilic inflammation.
METHODS: Wild-type (WT) BALB/c and eosinophil deficient (PHIL) mice were sensitized to house dust mite (HDM) using a chronic exposure protocol and treated with AMD3100 to modulate SDF-1 stimulated progenitor traffic. Following HDM challenge, lung-extracted EPCs were enumerated along with airway inflammation, microvessel density (MVD) and airway methacholine responsiveness (AHR).
RESULTS: Following Ag sensitization, both WT and PHIL mice exhibited HDM-induced increase in airway inflammation, EPC lung-accumulation, lung angiogenesis and AHR. Treatment with AMD3100 significantly attenuated outcome measures in both groups of mice. Significantly lower levels of EPC and a trend for lower vascularization were detected in PHIL versus WT mice.
CONCLUSIONS: This study shows that while allergen-induced lung-homing of endothelial progenitor cells, increased tissue vascularization and development lung dysfunction can occur in the absence of eosinophils, the presence of these cells worsens the pathology of the allergic response.

PMID: 25279605 [PubMed – as supplied by publisher]

View full post on pubmed: asthma

Exacerbation of asthma and airway infection: is the virus the villain?

Exacerbation of asthma and airway infection: is the virus the villain?

J Pediatr (Rio J). 2014 Sep 24;

Authors: Costa LD, Costa PS, Camargos PA

Abstract
OBJECTIVE: to review the available literature on the association between acute viral respiratory tract infection and the onset of asthma exacerbations, identifying the most prevalent viruses, detection methods, as well as preventive and therapeutic aspects.
DATA SOURCE: a search was conducted in PubMed, Lilacs, and SciELO databases, between the years 2002 and 2013, using the following descriptors: asthma exacerbation, virus, child, and acute respiratory infection.
DATA SYNTHESIS: a total of 42 original articles addressing the identification of respiratory viruses during episodes of asthma exacerbation were selected, mostly cross-sectional studies. There was a wide variation in the methodology of the assessed studies, particularly in relation to the children’s age and methods of collection and viral detection. The results indicate that, in up to 92.2% of exacerbations, a viral agent was potentially the main triggering factor, and human rhinovirus was the most frequently identified factor. The pattern of viral circulation may have been responsible for the seasonality of exacerbations. The association between viral infections and allergic inflammation appears to be crucial for the clinical and functional uncontrolled asthma, but few studies have evaluated other triggering factors in association with viral infection.
CONCLUSIONS: respiratory viruses are present in the majority of asthmatic children during episodes of exacerbation. The involved physiopathological mechanisms are yet to be fully established, and the synergism between allergic inflammation and viral infection appears to determine uncontrolled disease. The role of other triggering and protective agents is yet to be clearly determined.

PMID: 25261603 [PubMed – as supplied by publisher]

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Airway Muscle-On-A-Chip Could Lead To Better Asthma Treatments – Headlines & Global News


Headlines & Global News

Airway Muscle-On-A-Chip Could Lead To Better Asthma Treatments
Headlines & Global News
"Every year asthma costs many tens of billions of dollars, significant productivity due to lost work and school days, and even lives," said senior author Kevin Kit Parker, Tarr Family Professor of Bioengineering and Applied Physics at the Harvard

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Airway muscle-on-a-chip to aid in search for new asthma treatments – Gizmag


Gizmag

Airway muscle-on-a-chip to aid in search for new asthma treatments
Gizmag
Unfortunately for asthma sufferers and those looking to develop new treatments to help them, animal models traditionally used to test potential new drugs don't always mimic human responses. Joining lungs and guts, scientists at Harvard's Wyss Institute
Airway muscle-on-a-chip 'simulates asthma in humans'Medical News Today
Harvard-made lung muscle could yield asthma insightsCNET
Airway Muscle-On-A-Chip Could Lead To Better Asthma TreatmentsHeadlines & Global News
Harvard School of Engineering and Applied Sciences
all 15 news articles »

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Airway muscle-on-a-chip ‘simulates asthma in humans’ – Medical News Today


Headlines & Global News

Airway muscle-on-a-chip 'simulates asthma in humans'
Medical News Today
Asthma affects more than 300 million people worldwide and is responsible for around 250,000 deaths every year. It is also a leading cause of emergency room visits and hospitalization among children. There are a number of medications that can help …
Airway Muscle-On-A-Chip Could Lead To Better Asthma TreatmentsHeadlines & Global News
Harvard-made lung muscle could yield asthma insightsCNET
Airway muscle-on-a-chip mimics asthmaHarvard School of Engineering and Applied Sciences
UPI.com
all 13 news articles »

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Airway muscle-on-a-chip mimics asthma – Harvard School of Engineering and Applied Sciences


Harvard School of Engineering and Applied Sciences

Airway muscle-on-a-chip mimics asthma
Harvard School of Engineering and Applied Sciences
Cambridge/Boston, Mass – September 23, 2014 – The majority of drugs used to treat asthma today are the same ones that were used 50 years ago. New drugs are urgently needed to treat this chronic respiratory disease, which causes nearly 25 million …

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Elderly asthma patients had greater airway involvement than younger patients – Healio

Elderly asthma patients had greater airway involvement than younger patients
Healio
Researchers in Japan conducted a retrospective analysis on 45 elderly patients (aged more than 65 years) with asthma (mean age, 73.1 years; 34 women; median disease duration, 12.7 years) and 67 nonelderly patients with asthma (mean age, 48.6 years; …

and more »

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