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Impact of sequential exposures to allergens and ultrafine particles on human bronchial epithelial BEAS-2B cells at the air liquid interface

ABSTRACT: BEAS-2B cells, at air liquid interface, were exposed to birch pollen extract or house dust mite extract in a cloud chamber and, later, to UFP rich combustion aerosols in an in vitro exposure system. As control the same exposure was performed without allergen containing extracts. The goal was to understand the effect of allergenic pre-exposure to a UFP rich combustion aerosol exposed cells and their effect on allergic sensitization, using an established model that mimics more closely real life exposures.

ORGANISM(S): Homo sapiens

PROVIDER: GSE216533 | GEO | 2023/03/01

REPOSITORIES: GEO

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Diet supplemented with polyphenol- and glucuronoxylan-rich fiber extract regulates colonic barrier function and cell proliferation in healthy rats

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Antigen specific human conventional T cells (CD154+) or regulatory T cells (CD137+) directed agains A. fumigatus or Birch pollen lysate isolated from Birch pollen allergic patients or healthy controls.

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2017-12-01 | PXD006196 | Pride

Comparative proteomics of common allergenic tree pollens of birch, alder and hazelComparative proteomics of common allergenic tree pollens of birch, alder and hazel

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A 6-month systems toxicology inhalation study in ApoE−/− mice demonstrates reduced cardiovascular effects of E-vapor aerosols compared to cigarette smoke.

Project description:Smoking cigarettes is harmful to the cardiovascular system. Considerable attention has been paid to the reduced harm potential of alternative nicotine-containing inhalable products such as e-cigarettes. We investigated the effects of E-vapor aerosols or cigarette smoke (CS) on atherosclerosis progression, cardiovascular function, and molecular changes in the heart and aorta of female ApoE−/− mice. The mice were exposed to aerosols from three different E-vapor formulations: (1) carrier (propylene glycol and vegetable glycerol), (2) base (carrier and nicotine) or (3) test (base and flavor) or to CS from 3R4F reference cigarettes for up to 6 months. Concentrations of CS and base or test aerosols were matched at 35 µg nicotine/L. Exposure to CS, compared with sham-exposed fresh air controls, accelerated atherosclerotic plaque formation, while no such effect was seen for any of the three E-vapor aerosols. Molecular changes indicated disease mechanisms related to oxidative stress and inflammation in general, plus changes in calcium regulation, and altered cytoskeletal organization and microtubule dynamics in the left ventricle. While ejection fraction, fractional shortening, cardiac output, and isovolumic contraction time remained unchanged following E-vapor aerosols exposure, the nicotine-containing base and test aerosols caused an increase in isovolumic relaxation time similar to CS. A nicotine-related increase in pulse wave velocity and arterial stiffness was also observed, but it was significantly lower for base and test aerosols than for CS. These results demonstrate that in comparison with CS, E-vapor aerosols induce substantially lower biological responses associated with smoking-related cardiovascular diseases.

2020-05-12 | E-MTAB-8578 | biostudies-arrayexpress

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