Human airway epithelial tight junctions

Godfrey, R. W. A.

doi:10.1002/(sici)1097-0029(19970901)38:5<488::aid-jemt5>3.0.co;2-e

Cited by 108 publications

(56 citation statements)

References 47 publications

(74 reference statements)

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“…As demonstrated by (ultra)structural and functional studies, hAELVi cells form tight intercellular junctions. Besides serving as a model of the tight alveolar air-blood barrier for drug transport and metabolism studies, they may also help to understand the role of tight junctions in disease development, since it is known that the alteration of tight junction integrity may be important for the course of infections, asthma and cystic fibrosis (Godfrey, 1997;Vermeer et al, 2009). Our results imply that hAELVi cells can be used in LLC and ALI conditions, for which the latter also allows deposition of aerosol particles or dry powder formulations in an existing set-up, the Pharmaceutical Aerosol Deposition Device on Cell Cultures (PADDOCC) (Hein et al, 2011).…”

Section: Referencesmentioning

confidence: 99%

Human alveolar epithelial cells expressing tight junctions to model the air-blood barrier

Kuehn

Kletting

Carvalho-Wodarz

et al. 2016

ALTEX

104

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Section: Referencesmentioning

confidence: 99%

Human alveolar epithelial cells expressing tight junctions to model the air-blood barrier

Kuehn

Kletting

Carvalho-Wodarz

et al. 2016

ALTEX

104

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“…The barrier function of an epithelial monolayer relies on tight junctions between adjacent cells, facilitated by zona occludens 1 (tight junction protein 1) and occludins, among other transmembrane proteins. 18 As these tight junctions fail in response to an environmental stressor, electrolytes are able to penetrate the gaps between cells more readily, and this can be measured by passing an electrical AC current through the cell monolayer and monitoring the impedance to the current. 19 Because the reduction of barrier function in the epithelium of the human airway can result in increased penetration of airborne particulates and subsequent pulmonary injury, edema, and infection, 20 barrier function is an important endpoint in toxicological studies of epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

Multiwalled carbon nanotubes induce altered morphology and loss of barrier function in human bronchial epithelium at noncytotoxic doses

Snyder¹,

Hussain²,

Rice³

et al. 2014

IJN

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Multiwalled carbon nanotubes (MWCNTs) have seen increasing application in consumer products over the past decade, resulting in an increasing risk of human exposure. While numerous toxicological studies have been performed using acute high doses of various carbonaceous nanomaterials, the effects of longer-term, low doses of MWCNTs remain relatively unexplored. This study examined bronchoscopy-derived healthy human bronchial epithelial cells exposed in submerged culture to noncytotoxic doses of MWCNTs over 7 days. Under these conditions, doses as low as 3 μg/mL caused altered cell morphology, superficially resembling fibroblasts. Electrical impedance of the epithelial monolayer was greatly reduced following MWCNT exposure. However, Western blot and polymerase chain reaction showed no elevated expression of the fibroblast markers, vimentin, α-smooth muscle actin, or fibronectin, indicating that a mechanism other than epithelial–mesenchymal transition may be responsible for the changes. Phalloidin and tubulin immunostaining showed disruption of the cytoskeleton, and confocal imaging showed a reduction of the tight junction proteins, zona occludens 1 and occludin. We propose that MWCNTs interfere with the cytoskeleton of the lung epithelium, which can result in a harmful reduction in barrier function over time, even at noncytotoxic doses.

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“…Therefore, nonmicrobial factors, such as ozone, that decrease epithelial barrier function could assist respiratory pathogens in establishing infection in the lung (44). In addition, patients with lung diseases such as asthma and smokinginduced bronchitis demonstrate increased airway epithelial permeability, and this may also affect bacterial infection and inflammatory responses (45)(46)(47)(48). Conversely, airway epithelia may provide an important "watchtower" function by amplifying inflammation when the airway mucosal barrier is breached.…”

Section: Discussionmentioning

confidence: 99%

Paracellular Permeability Restricts Airway Epithelial Responses to Selectively Allow Activation by Mediators at the Basolateral Surface

Humlicek

Manzel

Chin

et al. 2007

The Journal of Immunology

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Respiratory pathogens and toxins often assault the lung from the airway lumen. Airway epithelia may initiate and amplify inflammation in response to these attacks, but under certain conditions confinement of inflammation to the airway lumen may be beneficial to the host. Accordingly, we hypothesized that airway epithelial polarity allows different responses to basolateral vs apical stimuli that may modulate inflammation. Using primary human airway epithelial cells differentiated at an air-liquid interface in culture, we found that responses to several cytokines required basolateral mediator application. In contrast, responses to Haemophilus influenzae occurred after either basolateral or apical interaction with airway epithelia. Experiments focused on IFN-γ receptor polarity confirmed its predominant basolateral location in cultured airway epithelia as well as in normal human airway tissue. Furthermore, physical and pharmacologic disruption of barrier function in airway epithelia allowed responses to apical application of IFN-γ and other cytokines. These in vitro studies directly correlated with experiments in mice in which an airway epithelial response to IFN-γ injected into the airway lumen was seen only after disruption of barrier function. The results indicate that airway epithelia with intact barrier function restrict inflammatory responses by limitation of cell activation through requiring interaction of selected mediators with the basolateral surface. However, loss of barrier integrity allows epithelial responses to these mediators if located in the airway lumen to amplify airway defenses.

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Human airway epithelial tight junctions

Cited by 108 publications

References 47 publications

Human alveolar epithelial cells expressing tight junctions to model the air-blood barrier

Human alveolar epithelial cells expressing tight junctions to model the air-blood barrier

Multiwalled carbon nanotubes induce altered morphology and loss of barrier function in human bronchial epithelium at noncytotoxic doses

Paracellular Permeability Restricts Airway Epithelial Responses to Selectively Allow Activation by Mediators at the Basolateral Surface

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