Effect of sub-chronic exposure to cigarette smoke, electronic cigarette and waterpipe on human lung epithelial barrier function

Ghosh, Baishakhi; Reyes-Caballero, Hermes; Akgün-Ölmez, Sevcan Gül; Nishida, Kristine; Chandrala, Lakshmana; Smirnova, Lena; Biswal, Shyam; Sidhaye, Venkataramana K.

doi:10.1186/s12890-020-01255-y

Cited by 32 publications

(39 citation statements)

References 59 publications

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“…E-cadherin is a principal component of the adherens junction and critical in maintaining cell-cell adhesion (18, 25–27). We and others have generated in vitro , animal, and human data indicating that loss of E-cadherin occurs after chronic tobacco exposure and in COPD patients (4–6, 16, 28). However, evidence that this loss of E-cadherin is not simply associated with disease but has a causal role in tissue remodeling in the adult lung and can serve as a therapeutic target to abrogate or reverse disease is lacking.…”

Section: Discussionmentioning

confidence: 99%

“…Primary non-diseased human bronchial epithelial (NHBE) and COPD human bronchial epithelial (CHBE) cells were purchased from MatTek Life Sciences (Ashland, MA, USA) or Lonza (Basel, Switzerland) were expanded on collagen-coated T 75 flask and differentiated into pseudostratified epithelium at air-liquid interface (ALI) on 0.4 µm pore size polyester membrane Transwells as described by us before (4–6).…”

Section: Methodsmentioning

confidence: 99%

“…The NHBEs at 4 to 6 weeks ALI were exposed to either exposed to CS smoke or humidified air for 10 days as mentioned previously by us(4–6). One CS exposure consisted of 2 cigarettes which burned for ∼ 8 minutes using the ISO puff regimen.…”

Section: Methodsmentioning

confidence: 99%

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Knockout of E-cadherin in adult mouse epithelium results in emphysema and airway disease

Ghosh

Loube

Thapa³

et al. 2021

Preprint

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Chronic obstructive pulmonary disease (COPD) is a devastating lung disease, characterized by a progressive decline in lung function, alveolar loss (emphysema), and airflow limitation due to excessive mucus secretion (chronic bronchitis), that can occur even after the injurious agent is removed. It is slated to rise to the 3rd leading cause of death due to chronic disease by 2030 globally, and the 4th leading cause of death due to chronic disease in the USA. While there is substantial evidence indicating loss of E-cadherin in the lung epithelium of patients with COPD, it is not known if this is causal to the disease. We investigated if loss of E-cadherin can result in lung disease using in both in vitro models of primary, differentiated human cells and in mouse models. Using a cell type-specific promoter using Cre/LoxP mice system to knock-out E-cadherin in ciliated and alveolar epithelial cell (Type 1 and Type 2) populations in adult mouse models, we determined that loss of E-cadherin caused airspace enlargement, as well as increased airway hyperresponsiveness indicating that it does have a causative role in causing COPD. Strategies to upregulate CDH1 (encodes for E-cadherin) in CHBEs and cigarette-smoke injured NHBEs can rescue the dysfunctional epithelium.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Knockout of E-cadherin in adult mouse epithelium results in emphysema and airway disease

Ghosh

Loube

Thapa³

et al. 2021

Preprint

Self Cite

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“…Some groups have reported regular washing of apical compartments for mucous clearing at weekly intervals during culture maintenance phases, as well as days prior to exposure to minimize confounding [ 172 , 173 ]. Longer-term exposure studies involving cigarette smoke or electronic cigarette aerosol involve intermittent exposures conducted over time intervals not longer than a couple of weeks; such intervals may not be long enough for mucus accumulation to become a significant issue, and regular washing protocols are not reported [ 174 , 175 , 176 ].…”

Section: Leveraging Airway On-chip Technology For Inhalation Assaysmentioning

confidence: 99%

“…Barrier-function-related-genes, such as those coding for apical junction proteins, have been used to assess differences in barrier integrity with stimulation [ 21 ]. Augmentation of such assessment with direct measurements is ideal, if available, as statistically significant differences evidenced by FITC-dextran or TEER are not always mirrored exactly in junction protein expression [ 175 ]. Transcriptomics is a promising application to microfluidic chips; lysis buffers can be injected into cell-containing channels and lysates can be collected as effluents.…”

Section: Readouts From Lung-on-a-chip Modelsmentioning

confidence: 99%

Airway-On-A-Chip: Designs and Applications for Lung Repair and Disease

Bennet

Randhawa

Hua

et al. 2021

Cells

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The lungs are affected by illnesses including asthma, chronic obstructive pulmonary disease, and infections such as influenza and SARS-CoV-2. Physiologically relevant models for respiratory conditions will be essential for new drug development. The composition and structure of the lung extracellular matrix (ECM) plays a major role in the function of the lung tissue and cells. Lung-on-chip models have been developed to address some of the limitations of current two-dimensional in vitro models. In this review, we describe various ECM substitutes utilized for modeling the respiratory system. We explore the application of lung-on-chip models to the study of cigarette smoke and electronic cigarette vapor. We discuss the challenges and opportunities related to model characterization with an emphasis on in situ characterization methods, both established and emerging. We discuss how further advancements in the field, through the incorporation of interstitial cells and ECM, have the potential to provide an effective tool for interrogating lung biology and disease, especially the mechanisms that involve the interstitial elements.

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Microphysiological Models of Lung Epithelium‐Alveolar Macrophage Co‐Cultures to Study Chronic Lung Disease

Lagowala,

Wally,

Wilmsen

et al. 2023

Advanced Biology

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The interactions between immune cells and epithelial cells influence the progression of many respiratory diseases, such as chronic obstructive pulmonary disease (COPD). In vitro models allow for the examination of cells in controlled environments. However, these models lack the complex 3D architecture and vast multicellular interactions between the lung resident cells and infiltrating immune cells that can mediate cellular response to insults. In this study, three complementary microphysiological systems are presented to delineate the effects of cigarette smoke and respiratory disease on the lung epithelium. First, the Transwell system allows the co‐culture of pulmonary immune and epithelial cells to evaluate cellular and monolayer phenotypic changes in response to cigarette smoke exposure. Next, the human and mouse precision‐cut lung slices system provides a physiologically relevant model to study the effects of chronic insults like cigarette smoke with the dissection of specific interaction of immune cell subtypes within the structurally complex tissue environment. Finally, the lung‐on‐a‐chip model provides an adaptable system for live imaging of polarized epithelial tissues that mimic the in vivo environment of the airways. Using a combination of these models, a complementary approach is provided to better address the intricate mechanisms of lung disease.

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Effect of sub-chronic exposure to cigarette smoke, electronic cigarette and waterpipe on human lung epithelial barrier function

Cited by 32 publications

References 59 publications

Knockout of E-cadherin in adult mouse epithelium results in emphysema and airway disease

Knockout of E-cadherin in adult mouse epithelium results in emphysema and airway disease

Airway-On-A-Chip: Designs and Applications for Lung Repair and Disease

Microphysiological Models of Lung Epithelium‐Alveolar Macrophage Co‐Cultures to Study Chronic Lung Disease

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