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

doi:10.1016/j.chemosphere.2019.125087

Cited by 21 publications

(33 citation statements)

References 71 publications

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“…The International Centre of Advanced Study in Environment, Ecosystem and Human Health (CISAS) project aimed at investigating environmental pollution and its connection with the ecosystem and human health, monitoring pollutant concentrations in human tissues and also performing in vitro/ex vivo experiments [7][8][9][10]. The CISAS project also included the extensive characterization of entire environmental matrices as well as food chains in three ICSs in southern Italy [11].…”

Section: Introductionmentioning

confidence: 99%

The Neonatal Environment and Health Outcomes (NEHO) Birth Cohort Study: Behavioral and Socioeconomic Characteristics and Drop-Out Rate from a Longitudinal Birth Cohort in Three Industrially Contaminated Sites in Southern Italy

Ruggieri

Maltese

Drago

et al. 2021

IJERPH

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Pregnant women living in industrially contaminated sites (ICSs) are exposed to environmental contaminants through different pathways, and thus children’s health may be affected by pollutants. We created the Neonatal Environment and Health Outcomes (NEHO) longitudinal birth cohort in three ICSs in the Mediterranean area of southern Italy, collecting comprehensive information on personal data and lifestyles by questionnaire. Through multiple correspondence analysis, we identified possible clusters of enrolled women, and a neural network classifier analysis (NNCA) was performed to identify variables capable of predicting the attrition rate of the study. NEHO recruited 845 mother–child pairs over two years. The mothers’ mean age was 31.1 ± 5.2 SD years. We found significant differences in socioeconomic status (SES) among the three evaluated ICS, and an overall 11.1% prevalence of mothers who actively smoked during pregnancy. Active smoking during pregnancy was strongly associated with the lowest socioeconomic level (p < 0.0001). By means of the NNCA, we found that smoking during pregnancy and the lowest education level characterized the cluster with the highest attrition rate (p < 0.001). Our results demonstrate that reason for public health concern still exists regarding smoking during pregnancy and that SES influences both lifestyles, producing negative pregnancy outcomes and a higher survey attrition rate.

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Section: Introductionmentioning

confidence: 99%

The Neonatal Environment and Health Outcomes (NEHO) Birth Cohort Study: Behavioral and Socioeconomic Characteristics and Drop-Out Rate from a Longitudinal Birth Cohort in Three Industrially Contaminated Sites in Southern Italy

Ruggieri

Maltese

Drago

et al. 2021

IJERPH

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“…The TER measurements were normalized by the area of the monolayer and given as cm 2 . Untreated 16HBE cells have been reported to have a TER around 600 Ω. cm 2 (Yuan et al, 2020), while A549 cells have been reported to have a TER around 175 Ω. cm 2 (Albano et al, 2020).…”

Section: Transepithelial Electrical Resistance (Ter) Measurementmentioning

confidence: 99%

miR-4456/CCL3/CCR5 Pathway in the Pathogenesis of Tight Junction Impairment in Chronic Obstructive Pulmonary Disease

Ding

et al. 2021

Front. Pharmacol.

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Background: Cigarette smoke exposure (CSE) is a major cause of chronic obstructive pulmonary disease (COPD). The smoke disrupts cell-cell adhesion by inducing epithelial barrier damage to the tight junction (TJ) proteins. Even though the inflammatory mechanism of chemokine (C-C motif) ligand 3 (CCL3) in COPD has gained increasing attention in the research community, however, the underlying signaling pathway, remains unknown.Objectives: To identify the relationship of CCL3 in the pathogenesis of tight junction impairment in COPD and the pathway through which CSE causes damage to TJ in COPD via CCL3, both in vivo and in vitro.Methods: We screened the inflammatory factors in the peripheral blood mononuclear cells (PBMCs) from healthy controls and patients at each GOLD 1-4 stage of chronic obstructive pulmonary disease. RT-PCR, western blot, and ELISA were used to detect the levels of CCL3, ZO-1, and occludin after Cigarette smoke exposure. Immunofluorescence was applied to examine the impairment of the TJs in 16-HBE and A549 cells. The reverse assay was used to detect the effect of a CCR5 antagonist (DAPTA) in COPD. In the CSE-induced COPD mouse model, H&E staining and lung function tests were used to evaluate the pathological and physical states in each group. Immunofluorescence was used to assess the impairment of TJs in each group. ELISA and RT-PCR were used to examine the mRNA or protein expression of CCL3 or miR-4456 in each group.Results: The in vivo and in vitro results showed that CCL3 expression was increased in COPD compared with healthy controls. CCL3 caused significant injury to TJs through its C-C chemokine receptor type 5 (CCR5), while miR-4456 could suppress the effect of CCL3 on TJs by binding to the 3′-UTR of CCL3.Conclusion: miR-4456/CCL3/CCR5 pathway may be a potential target pathway for the treatment of COPD.

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“…Airway epithelium provides a biological barrier and prevents exogenous substances from entering airway mucosa [9]. Indeed, it represents the first line of defense against potential pathogens or noxious agents, promoting oxidative stress, activation of inflammatory cells, the release of inflammatory mediators such as reactive oxygen species (ROS) and cytokines in epithelial cells [10,11]. The epithelium is a monolayer of polarized epithelial cells maintained by the formation of tight (as zonula occludens (ZO)-1 and Claudins) and adherent junctions (as the transmembrane protein E-cadherin), involved in barrier functions and integrity [12,13].…”

Section: Introductionmentioning

confidence: 99%

“…The epithelium is a monolayer of polarized epithelial cells maintained by the formation of tight (as zonula occludens (ZO)-1 and Claudins) and adherent junctions (as the transmembrane protein E-cadherin), involved in barrier functions and integrity [12,13]. Pollutants induce pulmonary toxicity, promoting a proinflammatory response that disturbs tissue homeostasis via multiple mechanisms, including apoptosis, oxidative stress, DNA damage/repair mechanisms and DNA demethylation disrupting E-cadherin-mediated cell adhesion in lung cells [10,14,15].…”

Section: Introductionmentioning

confidence: 99%

Cadmium and Cadmium/BDE (47 or 209) Exposure Affect Mitochondrial Function, DNA Damage/Repair Mechanisms and Barrier Integrity in Airway Epithelial Cells

et al. 2022

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Heavy metals and Brominated diphenyl ether flame-retardants (BDEs) often coexist in the environment and are capable of inducing injury, cytotoxicity or genotoxicity in human epithelial cells of the lung. We studied the effects of single Cadmium chloride (CdCl2) or CdCl2/BDE (47 or 209) mixtures in airway epithelial cells, using A549 cell line cultured at submerged conditions and air–liquid interface (ALI) (an in vitro model described as physiologically relevant in vivo-like). We evaluated cell viability, oxidative stress, apoptosis, DNA damage/repair (Comet assay, γH2AX phosphorylation ser139), mitochondrial redox balance (NOX-4, Nrf2 and TFAM) and cell barrier integrity (TEER, ZO-1, Claudin-1, E-cadherin-1) in A549 cells exposed to CdCl2 (1 nM to 10 µM), or to CdCl2 (100 nM)/BDEs (47 or 209) (100 nM). CdCl2 (10 μM) reduced cell viability and increased apoptosis. CdCl2 (100 nM) significantly affected DNA-damage/repair (Olive Tail length production), γH2AX phosphorylation and oxidative stress (ROS/JC-1 production) in submerged cell cultures. CdCl2 (100 nM) decreased viability, TEER, ZO-1, Claudin-1 and E-cadherin-1 mRNA expression, and Nrf2 and TFAM while increased NOX-4, in ALI culture of cells. In both cell culture approaches, the cells stimulated with Cadmium/BDEs mixtures did not show a significant increase in the effects observed in the cells treated with CdCl2 alone. CdCl2 inhalation might exert cytotoxicity and genotoxicity, playing a pivotal role in the uncontrolled oxidative stress, damaging DNA and gene expression in airway epithelial cells. No additional or synergistic adverse effects of CdCl2/BDEs mixture were observed in comparison to CdCl2 alone in lung epithelium.

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

Cited by 21 publications

References 71 publications

The Neonatal Environment and Health Outcomes (NEHO) Birth Cohort Study: Behavioral and Socioeconomic Characteristics and Drop-Out Rate from a Longitudinal Birth Cohort in Three Industrially Contaminated Sites in Southern Italy

The Neonatal Environment and Health Outcomes (NEHO) Birth Cohort Study: Behavioral and Socioeconomic Characteristics and Drop-Out Rate from a Longitudinal Birth Cohort in Three Industrially Contaminated Sites in Southern Italy

miR-4456/CCL3/CCR5 Pathway in the Pathogenesis of Tight Junction Impairment in Chronic Obstructive Pulmonary Disease

Cadmium and Cadmium/BDE (47 or 209) Exposure Affect Mitochondrial Function, DNA Damage/Repair Mechanisms and Barrier Integrity in Airway Epithelial Cells

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