Can PBDEs affect the pathophysiologic complex of epithelium in lung diseases?

6533b837fe1ef96bd12a27b9

RESEARCH PRODUCT

Can PBDEs affect the pathophysiologic complex of epithelium in lung diseases?

Albano Giusy Daniela Moscato Monica Montalbano Angela Marina Anzalone Giulia Gagliardo Rosalia Bonanno Anna Giacomazza Daniela Barone Rosario Drago Gaspare Cibella Fabio Profita Mirella

subject

Lung Diseases Health Toxicology and Mutagenesis 0208 environmental biotechnology 02 engineering and technology 010501 environmental sciences Mucin 5AC BROMINATED FLAME RETARDANTS medicine.disease_cause 01 natural sciences Polybrominated diphenyl ethers PARTICULATE MATTER Electric Impedance Halogenated Diphenyl Ethers Flame Retardants Inhalation Tight junction AIRWAY MUCUS Chemistry General Medicine respiratory system Pollution Mucin-5B INTRACELLULAR GLUTATHIONE Polybrominated diphenyl ethers; Inflammation; Oxidative stress; Mucins; Epithelial barrier integrity; Rheological properties medicine.anatomical_structure NADPH Oxidase 4 medicine.symptom Environmental Engineering Inflammation Bronchi EXPOSURE SYSTEM Tight Junctions Andrology medicine Environmental Chemistry Humans Rheological properties Polybrominated diphenyl ether 0105 earth and related environmental sciences Aged Inflammation Epithelial barrier integrity POLYBROMINATED DIPHENYL ETHERS Mucin Interleukin-8 Mucins Public Health Environmental and Occupational Health Epithelial Cells General Chemistry N-ACETYLCYSTEINE Epithelium 020801 environmental engineering respiratory tract diseases Oxidative Stress A549 Cells Mucin EX-VIVO MODEL Oxidative stre Respiratory epithelium AEROSOL-PARTICLES Oxidative stress

description

Brominated flame-retardant (BFRs) exposure promotes multiple adverse health outcomes involved in oxidative stress, inflammation, and tissues damage. We investigated BFR effects, known as polybrominated diphenyl ethers (PBDEs) (47, 99 and 209) in an air-liquid-interface (ALI) airway tissue derived from A549 cell line, and compared with ALI culture of primary human bronchial epithelial cells (pHBEC). The cells, exposed to PBDEs (47, 99 and 209) (0.01-1 mu M) for 24 h, were studied for IL-8, Muc5AC and Muc5B (mRNAs and proteins) production, as well as NOX-4 (mRNA) expression. Furthermore, we evaluated tight junction (TJ) integrity by Trans-Epithelial Electrical Resistance (TEER) measurements, and zonula occludens-1 (ZO-1) expression in the cells, and pH variations and rheological properties (elastic G', and viscous G `', moduli) in apical washes of ALI cultures. N-acetylcysteine (NAC) (10 mM) effects were tested in our experimental model of A549 cells. PBDEs (47, 99 and 209) exposure decreased TEER, ZO-1 and pH values, and increased IL-8, Muc5AC, Muc5B (mRNAs and proteins), NOX-4 (mRNA), and rheological parameters (G', G `') in ALI cultures of A549 cell line and pHBEC. NAC inhibited PBDE effects in A549 cells. PBDE inhalation might impairs human health of the lungs inducing oxidative stress, inflammatory response, loss of barrier integrity, unchecked mucus production, as well as altered physicochemical and biological properties of the fluids in airway epithelium. The treatment with anti-oxidants restored the negative effects of PBDEs in epithelial cells. (C) 2019 Elsevier Ltd. All rights reserved.

year	journal	country	edition	language
2020-01-01	Chemosphere

10.1016/j.chemosphere.2019.125087 https://pubmed.ncbi.nlm.nih.gov/31622892