Calu-3: a human airway epithelial cell line that shows cAMP-dependent Cl- secretion

Shen, B. Q.; Finkbeiner, Walter E.; Wine, Jeffrey J.; Mrsny, Randall J.; Widdicombe, Jonathan

doi:10.1152/ajplung.1994.266.5.l493

Cited by 274 publications

(352 citation statements)

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“…Thus, these observations conflict with previous reports suggesting CFTR is the predominant mediator of gland acinar secretion, based on high CFTR immunolocalization signals in acinar serous cells (Engelhardt et al, 1992), studies of agonist regulation of porcine and human gland secretion rates (Joo et al, 2002;Ballard and Inglis, 2004), and studies of CalU-3 cells, which have been used as a model system of acinar serous cells (Shen et al, 1994).…”

Section: Function Of Glands In Airway Fluid Balancecontrasting

confidence: 87%

Characterization of Wild-Type and ΔF508 Cystic Fibrosis Transmembrane Regulator in Human Respiratory Epithelia

Kreda

Mall

Mengos

et al. 2005

MBoC

234

210

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Previous studies in native tissues have produced conflicting data on the localization and metabolic fate of WT and ⌬F508 cystic fibrosis transmembrane regulator (CFTR) in the lung. Combining immunocytochemical and biochemical studies utilizing new high-affinity CFTR mAbs with ion transport assays, we examined both 1) the cell type and region specific expression of CFTR in normal airways and 2) the metabolic fate of ⌬F508 CFTR and associated ERM proteins in the cystic fibrosis lung. Studies of lungs from a large number of normal subjects revealed that WT CFTR protein localized to the apical membrane of ciliated cells within the superficial epithelium and gland ducts. In contrast, other cell types in the superficial, gland acinar, and alveolar epithelia expressed little WT CFTR protein. No ⌬F508 CFTR mature protein or function could be detected in airway specimens freshly excised from a large number of ⌬F508 homozygous subjects, despite an intact ERM complex. In sum, our data demonstrate that WT CFTR is predominantly expressed in ciliated cells, and ⌬F508 CFTR pathogenesis in native tissues, like heterologous cells, reflects loss of normal protein processing.

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Section: Function Of Glands In Airway Fluid Balancecontrasting

confidence: 87%

Characterization of Wild-Type and ΔF508 Cystic Fibrosis Transmembrane Regulator in Human Respiratory Epithelia

Kreda

Mall

Mengos

et al. 2005

MBoC

234

210

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“…Calu3 cells were specifically selected for this assay, on the basis of their ability to form a tight barrier. 51 Although several factors play a role in recovery of injured epithelium, KGF promotes epithelial protection in mouse and human studies of lung 26,52,53 and skin 27 injury. AT-RvD3 increased KGF levels in both BALF and whole lung lysates, suggesting a link for the SPM to this key protective signaling circuit for wounded epithelium.…”

Section: Discussionmentioning

confidence: 99%

Resolvin D3 and Aspirin-Triggered Resolvin D3 Are Protective for Injured Epithelia

Colby

Abdulnour

Sham

et al. 2016

The American Journal of Pathology

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Acute lung injury is a life-threatening condition caused by disruption of the alveolar-capillary barrier leading to edema, influx of inflammatory leukocytes, and impaired gas exchange. Specialized proresolving mediators biosynthesized from essential fatty acids, such as docosahexaenoic acid, have tissue protective effects in acute inflammation. Herein, we found that the docosahexaenoic acidederived mediator resolvin D3 (RvD3): 4S,11R,17S-trihydroxydocosa-5Z,7E,9E,13Z,15E,19Z-hexaenoic acid was present in uninjured lungs, and increased significantly 24 to 72 hours after hydrochloric acideinitiated injury. Because of its delayed enzymatic degradation, we used aspirin-triggered (AT)-RvD3: 4S,11R,17R-trihydroxydocosa-5Z,7E,9E,13Z,15E,19Z-hexaenoic acid, a 17R-epimer of RvD3, for in vivo experiments. Histopathological correlates of acid injury (alveolar wall thickening, edema, and leukocyte infiltration) were reduced in mice receiving AT-RvD3 1 hour after injury. AT-RvD3etreated mice had significantly reduced edema, as demonstrated by lower wet/dry weight ratios, increased epithelial sodium channel g expression, and more lymphatic vessel endothelial hyaluronan receptor 1-positive vascular endothelial growth factor receptor 3-positive lymphatic vessels. Evidence for counterregulation of NF-kB by RvD3 and AT-RvD3 was seen in vitro and by AT-RvD3 in vivo. Increases in lung epithelial cell proliferation and bronchoalveolar lavage fluid levels of keratinocyte growth factor were observed with AT-RvD3, which also promoted cutaneous re-epithelialization. Together, these data demonstrate protective actions of RvD3 and AT-RvD3 for injured mucosa that accelerated restoration of epithelial barrier and function. (Am J Pathol 2016 http://dx.doi.org/10.1016/j.ajpath.2016 Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are serious conditions characterized by loss of normal epithelial and endothelial barrier function, leading to pulmonary edema and infiltration of leukocytes culminating in significant impairments in gas exchange. 1 ARDS and its milder form, ALI, are serious conditions characterized by loss of normal epithelial and endothelial barrier function, leading to pulmonary edema and infiltration of leukocytes culminating in significant impairments in gas exchange. 1 ALI is a common condition, affecting approximately 200,000 patients a year in the United States alone. 2 Although our understanding of the pathophysiological changes associated with ALI/ARDS has improved since its original description, effective management of this condition still proves difficult, and mortality remains approximately 40%. 2 Aspiration pneumonia/pneumonitis is a common cause of ALI/ARDS characterized by direct damage to lung epithelia (because of the low pH of gastric contents) followed by extensive sloughing of the injured epithelial cells. 3 Despite significant damage to the epithelial barrier,

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“…An in vitro transport study was conducted using Calu-3 airway epithelial cells grown to confluency at an air-liquid interface to form intact monolayers capable of mimicking the mucosal cell layer in the bronchial region of the airways (Shen et al, 1994). The Calu-3 cells line has previously been used as a means of potentially predicting the transport of materials across the airway epithelium in vivo (Fiegel et al, 2003, Foster et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Liposome Encapsulation on the Pharmacokinetics of Recombinant Secretory Leukocyte Protease Inhibitor (rSLPI) Therapy after Local Delivery to a Guinea Pig Asthma Model

et al. 2011

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NG, Cryan SA. The effect of liposome encapsulation on the pharmacokinetics of recombinant secretory leukocyte protease inhibitor (rSLPI) therapy after local delivery to a guinea pig asthma model. Pharmaceutical Research. 2011;28(9):2233-45. AuthorsAileen Gibbons, Danielle Padilla-Carlin, Ciara Kelly, Anthony J. Hickey, Clifford Taggart, Noel G. McElvaney, and Sally-Ann Cryan This article is available at e-publications@RCSI: http://epubs.rcsi.ie/spharmart/3 -Use LicenceAttribution-Non-Commercial-ShareAlike 1.0 You are free:• to copy, distribute, display, and perform the work.• to make derivative works. Under the following conditions:• Attribution -You must give the original author credit.• Non-Commercial -You may not use this work for commercial purposes.• Share Alike -If you alter, transform, or build upon this work, you may distribute the resulting work only under a licence identical to this one. Methods: Transport of DOPS-rSLPI and free-rSLPI across a polarised air-liquid epithelial monolayer was measured. An asthma guinea pig model was administered either DOPS-rSLPI liposomes or free-rSLPI by intratracheal instillation. Results: Apparent permeability (P app ) of free-rSLPI was significantly higher at 4.9 x10 -6 cm/s than for DOPS-rSLPI, P app of 2.05 x10 -7 cm/s. In vivo studies confirmed this result. Plasma rSLPI concentrations were highest in free-rSLPI treated animals compared with those treated with DOPS-rSLPI, there also appeared to be a trend for higher intracellular rSLPI content in animals dosed with DOPS-rSLPI compared to free-rSLPI. Eosinophil influx was recorded as a measure of inflammation. Pre-dosing with either free-rSLPI or DOPSrSLPI prevented inflammatory response to antigen challenge to levels comparable to control animals. Conclusion: Encapsulation of rSLPI in DOPS:Chol liposomes improves stability, reduces clearance and increases residence time in the lungs after local delivery.3

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Calu-3: a human airway epithelial cell line that shows cAMP-dependent Cl- secretion

Cited by 274 publications

References 0 publications

Characterization of Wild-Type and ΔF508 Cystic Fibrosis Transmembrane Regulator in Human Respiratory Epithelia

Characterization of Wild-Type and ΔF508 Cystic Fibrosis Transmembrane Regulator in Human Respiratory Epithelia

Resolvin D3 and Aspirin-Triggered Resolvin D3 Are Protective for Injured Epithelia

The Effect of Liposome Encapsulation on the Pharmacokinetics of Recombinant Secretory Leukocyte Protease Inhibitor (rSLPI) Therapy after Local Delivery to a Guinea Pig Asthma Model

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