Mouse Infestations Cause More Asthma Symptoms than Cockroach Exposure – Newswise (press release)


Counsel & Heal

Mouse Infestations Cause More Asthma Symptoms than Cockroach Exposure
Newswise (press release)
Past research has been inconsistent in determining the relative effects of mouse droppings vs. cockroach exposure on asthma in children. According to a study being presented at the American College of Allergy, Asthma and Immunology (ACAAI) Annual …
Does father really know best? Maybe not when it comes to controlling asthmaMedical Xpress
Caregivers are not Educated enough about Asthma ManagementCounsel & Heal
Exposure to indoor air pollution affects children's lungsNews-Medical.net
Zee News –TIME
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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.

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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]

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Mouse Study Finds Prenatal Stress Increases Asthma Risk in Child – PsychCentral.com


PsychCentral.com

Mouse Study Finds Prenatal Stress Increases Asthma Risk in Child
PsychCentral.com
Now, a new study finds that prenatal stress may also be linked to the development of asthma. Researchers at the Harvard School of Public Health found that stress among pregnant mice — even a single bout — led to an increased risk of allergy-induced …

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Cytokine profile of bronchoalveolar lavage fluid from a mouse model of bronchial asthma during seasonal H1N1 infection.

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Cytokine profile of bronchoalveolar lavage fluid from a mouse model of bronchial asthma during seasonal H1N1 infection.

Cytokine. 2014 Jul 3;69(2):206-210

Authors: Hasegawa S, Wakiguchi H, Okada S, Gui Kang Y, Fujii N, Hasegawa M, Hasegawa H, Ainai A, Atsuta R, Shirabe K, Toda S, Wakabayashi-Takahara M, Morishima T, Ichiyama T

Abstract
BACKGROUND: Several studies support the role of viral infections in the pathogenesis of asthma exacerbation. However, several pediatricians believe that influenza virus infection does not exacerbate bronchial asthma, except for influenza A H1N1 2009 pandemic [A(H1N1)pdm09] virus infection. We previously reported that A(H1N1)pdm09 infection possibly induces severe pulmonary inflammation or severe asthmatic attack in a mouse model of bronchial asthma and in asthmatic children. However, the ability of seasonal H1N1 influenza (H1N1) infection to exacerbate asthmatic attacks in bronchial asthma patients has not been previously reported, and the differences in the pathogenicity profiles, such as cytokine profiles, remains unclear in bronchial asthma patients after A(H1N1)pdm09 and H1N1 infections.
METHODS: The cytokine levels and viral titers in the bronchoalveolar lavage (BAL) fluid from mice with and without asthma after H1N1 infection (A/Yamagata and A/Puerto Rico strains) were compared.
RESULTS: The interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-?, IL-5, interferon (IFN)-?, IFN-?, and IFN-? levels were significantly higher in the BAL fluids from the control/H1N1 mice than from the asthmatic/H1N1 mice. The viral titers in the BAL fluid were also significantly higher in the control/H1N1mice than in the asthmatic/H1N1 mice infected with either A/Yamagata or A/Puerto Rico.
CONCLUSIONS: A(H1N1)pdm09 infection, but not H1N1 infection, can induce severe pulmonary inflammation through elevated cytokine levels in a mouse model of asthma.

PMID: 24998935 [PubMed – as supplied by publisher]

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Maternal vitamin A deficiency linked to postnatal asthma: Mouse data – NutraIngredients.com


Science Codex

Maternal vitamin A deficiency linked to postnatal asthma: Mouse data
NutraIngredients.com
The mouse study, published in the Journal of Clinical Investigation, provides evidence that a lack of vitamin A during pregnancy is linked to postnatal airway hyperresponsiveness, which is a hallmark of asthma. Led by Dr Wellington Cardoso from
Prenatal vitamin A deficiency tied to postnatal asthmaEurekAlert (press release)
First evidence of link between prenatal vitamin A deficiency and postnatal asthmaNews-Medical.net

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Can Salmonella Lower Asthma Risk? Hygiene Hypothesis Upheld In Mouse … – Medical Daily


Medical Daily

Can Salmonella Lower Asthma Risk? Hygiene Hypothesis Upheld In Mouse
Medical Daily
Prior research into Salmonella's impact on allergies has shown that children who were infected had lower rates of asthma later in life than other adults who were never infected as kids. The mechanism of the present study is the same in mice models
Salmonella Infections Reduce Asthma AttacksGenetic Engineering News
Could asthma be treated with PROBIOTICS? Bug that mimics salmonella could Daily Mail
Salmonella Infection Mitigates AsthmaLaboratory Equipment

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Using Asthma Medication, Scientists Improve Cognitive Function in Mouse … – Medical Daily

Using Asthma Medication, Scientists Improve Cognitive Function in Mouse
Medical Daily
New research at the Stanford University School of Medicine found that an existing, FDA-approved form of asthma medication called formoterol improved cognitive functions in a mouse model of Down syndrome. Science Daily reports that by activating certain 

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Are mouse models of asthma appropriate for investigating the pathogenesis of airway hyper-responsiveness?

Are mouse models of asthma appropriate for investigating the pathogenesis of airway hyper-responsiveness?

Front Physiol. 2012;3:312

Authors: Kumar RK, Foster PS

Abstract
Whether mouse models of chronic asthma can be used to investigate the relationship between airway inflammation/remodeling and airway hyper-responsiveness (AHR) is a vexed question. It raises issues about the extent to which such models replicate key features of the human disease. Here, we review some of the characteristic pathological features of human asthma and their relationship to AHR and examine some limitations of mouse models that are commonly used to investigate these relationships. We compare these conventional models with our mouse model of chronic asthma involving long-term low-level inhalational challenge and review studies of the relationship between inflammation/remodeling and AHR in this model and its derivatives, including models of an acute exacerbation of chronic asthma and of the induction phase of childhood asthma. We conclude that while extrapolating from studies in mouse models to AHR in humans requires cautious interpretation, such experimental work can provide significant insights into the pathogenesis of airway responsiveness and its molecular and cellular regulation.

PMID: 23060800 [PubMed – in process]

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