Effects of early-life exposure to allergens and bacteria on recurrent wheeze and atopy in urban children.

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Effects of early-life exposure to allergens and bacteria on recurrent wheeze and atopy in urban children.

J Allergy Clin Immunol. 2014 May 28;

Authors: Lynch SV, Wood RA, Boushey H, Bacharier LB, Bloomberg GR, Kattan M, O’Connor GT, Sandel MT, Calatroni A, Matsui E, Johnson CC, Lynn H, Visness CM, Jaffee KF, Gergen PJ, Gold DR, Wright RJ, Fujimura K, Rauch M, Busse WW, Gern JE

Abstract
BACKGROUND: Wheezing illnesses cause major morbidity in infants and are frequent precursors to asthma.
OBJECTIVE: We sought to examine environmental factors associated with recurrent wheezing in inner-city environments.
METHODS: The Urban Environment and Childhood Asthma study examined a birth cohort at high risk for asthma (n = 560) in Baltimore, Boston, New York, and St Louis. Environmental assessments included allergen exposure and, in a nested case-control study of 104 children, the bacterial content of house dust collected in the first year of life. Associations were determined among environmental factors, aeroallergen sensitization, and recurrent wheezing at age 3 years.
RESULTS: Cumulative allergen exposure over the first 3 years was associated with allergic sensitization, and sensitization at age 3 years was related to recurrent wheeze. In contrast, first-year exposure to cockroach, mouse, and cat allergens was negatively associated with recurrent wheeze (odds ratio, 0.60, 0.65, and 0.75, respectively; P ? .01). Differences in house dust bacterial content in the first year, especially reduced exposure to specific Firmicutes and Bacteriodetes, was associated with atopy and atopic wheeze. Exposure to high levels of both allergens and this subset of bacteria in the first year of life was most common among children without atopy or wheeze.
CONCLUSIONS: In inner-city environments children with the highest exposure to specific allergens and bacteria during their first year were least likely to have recurrent wheeze and allergic sensitization. These findings suggest that concomitant exposure to high levels of certain allergens and bacteria in early life might be beneficial and suggest new preventive strategies for wheezing and allergic diseases.

PMID: 24908147 [PubMed – as supplied by publisher]

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New synthetic molecule can help prevent asthma attacks triggered by allergens – Tech Times


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New synthetic molecule can help prevent asthma attacks triggered by allergens
Tech Times
(Photo : Wikimedia Commons). Millions of Americans suffer from asthma, a chronic lung condition characterized by tightness on the chest, breathlessness, wheezing and coughing whenever the sufferer is exposed to certain allergens. A study conducted by a …
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Air Scrubber Plus Reduces Allergens and Germs That Aggravate Asthma and … – PR Web (press release)

Air Scrubber Plus Reduces Allergens and Germs That Aggravate Asthma and
PR Web (press release)
Air Scrubber Plus Reduces Allergens and Germs That Aggravate Asthma and Allergies. Air Scrubber Plus® recently announced a way to improve indoor air quality for those who suffer from asthma and allergies during Asthma and Allergy Awareness Month.

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Asthma Drug Helps Desensitize People To Multiple Food Allergens At Once – RedOrbit


RedOrbit

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Endotoxin Exposure during Sensitization to Blomia tropicalis Allergens Shifts TH2 Immunity Towards a TH17-Mediated Airway Neutrophilic Inflammation: Role of TLR4 and TLR2.

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Endotoxin Exposure during Sensitization to Blomia tropicalis Allergens Shifts TH2 Immunity Towards a TH17-Mediated Airway Neutrophilic Inflammation: Role of TLR4 and TLR2.

PLoS One. 2013;8(6):e67115

Authors: Barboza R, Câmara NO, Gomes E, Sá-Nunes A, Florsheim E, Mirotti L, Labrada A, Alcântara-Neves NM, Russo M

Abstract
Experimental evidence and epidemiological studies indicate that exposure to endotoxin lipopolysaccharide (eLPS) or other TLR agonists prevent asthma. We have previously shown in the OVA-model of asthma that eLPS administration during alum-based allergen sensitization blocked the development of lung TH2 immune responses via MyD88 pathway and IL-12/IFN-? axis. In the present work we determined the effect of eLPS exposure during sensitization to a natural airborne allergen extract derived from the house dust mite Blomia tropicalis (Bt). Mice were subcutaneously sensitized with Bt allergens co-adsorbed onto alum with or without eLPS and challenged twice intranasally with Bt. Cellular and molecular parameters of allergic lung inflammation were evaluated 24 h after the last Bt challenge. Exposure to eLPS but not to ultrapure LPS (upLPS) preparation during sensitization to Bt allergens decreased the influx of eosinophils and increased the influx of neutrophils to the airways. Inhibition of airway eosinophilia was not observed in IFN-?deficient mice while airway neutrophilia was not observed in IL-17RA-deficient mice as well in mice lacking MyD88, CD14, TLR4 and, surprisingly, TLR2 molecules. Notably, exposure to a synthetic TLR2 agonist (PamCSK4) also induced airway neutrophilia that was dependent on TLR2 and TLR4 molecules. In the OVA model, exposure to eLPS or PamCSK4 suppressed OVA-induced airway inflammation. Our results suggest that B. tropicalis allergens engage TLR4 that potentiates TLR2 signaling. This dual TLR activation during sensitization results in airway neutrophilic inflammation associated with increased frequency of lung TH17 cells. Our work highlight the complex interplay between bacterial products, house dust mite allergens and TLR signaling in the induction of different phenotypes of airway inflammation.

PMID: 23805294 [PubMed – as supplied by publisher]

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3 Common Allergens – How You Can Prevent Triggering an Allergy Attack – Hive Health Media


Hive Health Media

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Common Childhood Asthma Not Rooted in Allergens, Inflammation – Science Daily (press release)

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Science Daily (press release)
May 23, 2013 — Little is known about why asthma develops, how it constricts the airway or why response to treatments varies between patients. Now, a team of researchers at Weill Cornell Medical College, Columbia University Medical Center and SUNY

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