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Increasing Evidence for Small Airway Role in Asthma Intensity
Monthly Prescribing Reference Increasing Evidence for Small Airway Role in Asthma Intensity. (HealthDay News) – There is increasing evidence that the small airways contribute significantly to the clinical expression and severity of asthma, according to research published online Nov. |
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Research Supports Role of BMI in Incident Asthma in Children
Monthly Prescribing Reference (HealthDay News) – Overweight and obese children have a significantly increased risk of incident asthma, with evidence of a dose-response effect of elevated body mass index (BMI), according to a meta-analysis published online Nov. 12 in Obesity Reviews. |
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Research supports role of BMI in incident asthma in children
Medical Xpress (HealthDay)—Overweight and obese children have a significantly increased risk of incident asthma, with evidence of a dose-response effect of elevated body mass index (BMI), according to a meta-analysis published online Nov. 12 in Obesity Reviews. |
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Increasing evidence for small airway role in asthma intensity
Medical Xpress Maarten van den Berge, M.D., Ph.D., from the University of Groningen in the Netherlands, and colleagues reviewed the clinical relevance of small airway disease and its implications for the treatment of asthma. The researchers found that, based on … |
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Research Supports Role of BMI in Incident Asthma in Children
Doctors Lounge Overweight and obese children have a significantly increased risk of incident asthma, with evidence of a dose-response effect of elevated body mass index, according to a meta-analysis published online Nov. 12 in Obesity Reviews. TUESDAY, Nov. |
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Increasing Evidence for Small Airway Role in Asthma Intensity
Doctors Lounge TUESDAY, Nov. 20 (HealthDay News) — There is increasing evidence that the small airways contribute significantly to the clinical expression and severity of asthma, according to research published online Nov. 9 in Allergy. Maarten van den Berge, M.D … |
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Alveolar Macrophages Play a Key Role in Cockroach-Induced Allergic Inflammation via TNF-? Pathway.
PLoS One. 2012;7(10):e47971
Authors: Kim JY, Sohn JH, Choi JM, Lee JH, Hong CS, Lee JS, Park JW
Abstract
The activity of the serine protease in the German cockroach allergen is important to the development of allergic disease. The protease-activated receptor (PAR)-2, which is expressed in numerous cell types in lung tissue, is known to mediate the cellular events caused by inhaled serine protease. Alveolar macrophages express PAR-2 and produce considerable amounts of tumor necrosis factor (TNF)-?. We determined whether the serine protease in German cockroach extract (GCE) enhances TNF-? production by alveolar macrophages through the PAR-2 pathway and whether the TNF-? production affects GCE-induced pulmonary inflammation. Effects of GCE on alveolar macrophages and TNF-? production were evaluated using in vitro MH-S and RAW264.6 cells and in vivo GCE-induced asthma models of BALB/c mice. GCE contained a large amount of serine protease. In the MH-S and RAW264.7 cells, GCE activated PAR-2 and thereby produced TNF-?. In the GCE-induced asthma model, intranasal administration of GCE increased airway hyperresponsiveness (AHR), inflammatory cell infiltration, productions of serum immunoglobulin E, interleukin (IL)-5, IL-13 and TNF-? production in alveolar macrophages. Blockade of serine proteases prevented the development of GCE induced allergic pathologies. TNF-? blockade also prevented the development of such asthma-like lesions. Depletion of alveolar macrophages reduced AHR and intracellular TNF-? level in pulmonary cell populations in the GCE-induced asthma model. These results suggest that serine protease from GCE affects asthma through an alveolar macrophage and TNF-? dependent manner, reflecting the close relation of innate and adaptive immune response in allergic asthma model.
PMID: 23094102 [PubMed – in process]
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Differences in viral illness patterns play a role in asthma development in …
News-Medical.net Children living in low-income urban areas appear especially prone to developing asthma, possibly related to infections they acquire early in life. In a new study in The Journal of Infectious Diseases, available online, researchers from the University … |
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Opportunity for asthma role
Pharmacy News Debbie Rigby, a member of the National Asthma Council Australia's expert working group, and consultant pharmacist, said there was an opportunity for pharmacists to play an important role in helping asthma patients deal with allergies. “There needs to … |
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Role of female sex hormones, estradiol and progesterone, in mast cell behavior.
Front Immunol. 2012;3:169
Authors: Zierau O, Zenclussen AC, Jensen F
Abstract
Female sex hormones have long been suspected to have an effect on mast cell (MC) behavior. This assumption is based on the expression of hormone receptors in MCs as well as on the fact that many MC-related pathophysiological alterations have a different prevalence in females than in males. Further, serum IgE levels are much higher in allergic female mice compared to male mice. Ovariectomized rats developed less airway inflammation compared to sham controls. Following estrogen replacement ovariectomized rats re-established airway inflammation levels’ found in intact females. In humans, a much higher asthma prevalence was found in women at reproductive age as compared to men. Serum levels of estradiol and progesterone have been directly correlated with the clinical and functional features of asthma. Around 30-40% of women who have asthma experienced worsening of their symptoms during the perimenstrual phase, the so-called perimenstrual asthma. Postmenopausal women receiving hormone replacement therapy have an increased risk of new onset of asthma. Beside, estrus cycle dependent changes on female sex hormones are related to changes on MC number in mouse uterine tissue and estradiol and progesterone were shown to induce uterine MC maturation and degranulation. We will discuss here the currently available information concerning the role of these female sex hormones on MC behavior.
PMID: 22723800 [PubMed – in process]
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