Development of cystic fibrosis and noncystic fibrosis airway cell lines

Zabner, Joseph; Karp, Phil; Seiler, Michael P.; Phillips, Stacia L.; Mitchell, Calista J.; Saavedra, M. A.; Welsh, Michael J.; Klingelhutz, Aloysius J.

doi:10.1152/ajplung.00355.2002

Cited by 162 publications

(188 citation statements)

References 56 publications

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“…Treatment of CF mice by ASM inhibitors, such as amitriptyline and others tricyclic antidepressants, has been shown to reduce the degree of inflammation (Teichgraber, 2008;Becker, 2010). Notably, amitriptyline results in dose dependent inhibition of IL-8 transcription by bronchial epithelial cell lines IB3-1 and CuFi-1, infected with P.aeruginosa (Figure 3), consistent with the overall anti-inflammatory www.intechopen.com IB3-1 (human bronchial epithelial cell line) (Zeitlin, 1991) (A), CuFi-1 (F508del/F508del CFTR mutant genotype) (B) and NuLi-1 (C), (wild type CFTR) (Zabner, 2003) cell lines were treated with dexamethasone, at doses indicated in the figure, or solvent alone, for 24 hours and then infected with P.aeruginosa strain PAO1 (kindly provided by A. Prince, Columbia University, New York)(50CFU/cell) for 4 hours at 37° C. The inflammatory response was evaluated by studying the expression of mRNA of IL-8, measured by Real-time qPCR as described (Dechecchi, 2008) independent experiments, performed in duplicate.…”

Section: Amitriptyline Reduces Il-8 Gene Expression In Cf Bronchial Csupporting

confidence: 68%

Pharmacological Modulators of Sphingolipid Metabolism for the Treatment of Cystic Fibrosis Lung Inflammation

Dechecchi¹,

Nicolis²,

Mazzi³

et al. 2012

Cystic Fibrosis - Renewed Hopes Through Research

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Section: Amitriptyline Reduces Il-8 Gene Expression In Cf Bronchial Csupporting

confidence: 68%

Pharmacological Modulators of Sphingolipid Metabolism for the Treatment of Cystic Fibrosis Lung Inflammation

Dechecchi¹,

Nicolis²,

Mazzi³

et al. 2012

Cystic Fibrosis - Renewed Hopes Through Research

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“…Cell Culture and Treatment Conditions-The NuLi-1 cell line, an immortalized, nontransformed cell line derived from human airway epithelium of normal genotype, was a gift from Dr. J. Zabner (University of Iowa) (30). Normal human bronchial epithelial cells were obtained by endobronchial brushes from human subjects under a protocol approved by Case Western Reserve University Institutional Review Board.…”

Section: Methodsmentioning

confidence: 99%

Neuregulin-1-Human Epidermal Receptor-2 Signaling Is a Central Regulator of Pulmonary Epithelial Permeability and Acute Lung Injury

Finigan

Faress

Wilkinson

et al. 2011

Journal of Biological Chemistry

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The mechanisms behind the loss of epithelial barrier function leading to alveolar flooding in acute lung injury (ALI) are incompletely understood. We hypothesized that the tyrosine kinase receptor human epidermal growth factor receptor-2 (HER2) would be activated in an inflammatory setting and participate in ALI. Interleukin-1␤ (IL-1␤) exposure resulted in HER2 activation in human epithelial cells and markedly increased conductance across a monolayer of airway epithelial cells. Upon HER2 blockade, conductance changes were significantly decreased. Mechanistic studies revealed that HER2 trans-activation by IL-1␤ required a disintegrin and metalloprotease 17 (ADAM17)-dependent shedding of the ligand neuregulin-1 (NRG-1). In murine models of ALI, NRG-1-HER2 signaling was activated, and ADAM17 blockade resulted in decreased NRG-1 shedding, HER2 activation, and lung injury in vivo. Finally, NRG-1 was detectable and elevated in pulmonary edema fluid from patients with ALI. These results suggest that the ADAM17-NRG-1-HER2 axis modulates the alveolar epithelial barrier and contributes to the pathophysiology of ALI. Acute lung injury (ALI)3 is a severe clinical disorder with an annual incidence of ϳ200,000 and a mortality of 40% in the United States (1). Most commonly seen in the setting of sepsis (2-4), ALI is marked by disruption of the alveolar barrier, leukocyte activation, release of inflammatory cytokines, and hypercoagulability. The net effect is an increase in alveolar epithelial permeability, resulting in alveolar flooding with proteinrich edema and life-threatening hypoxemia (5). An intact epithelial barrier is essential to maintaining normal pulmonary fluid balance. Indeed, damage to the endothelium alone is insufficient to cause pulmonary edema, whereas epithelial injury results in severe lung injury (6 -8). The epithelium provides a greater resistance to proteins and fluid than the capillary endothelium and is responsible for the active ion transport-dependent removal of edema fluid from the distal air spaces of the lung (9 -11).The tyrosine kinase receptor human epidermal growth factor receptor-2 (HER2) is expressed by pulmonary bronchial epithelial cells and is involved in multiple physiologic processes, including cell proliferation and wound repair. The HER receptor family consists of four type 1, membrane-bound tyrosine kinase receptors: HER1 or epidermal growth factor receptor (EGFR), HER2, HER3, and HER4 (12). HER2 has no known ligand and requires partnering with another HER family member for activation. HER2 and 3 are highly expressed in pulmonary bronchial epithelial cells (compared with HER1 and 4) (13). HER3 is the receptor for the ligand neuregulin-1 (NRG-1), but HER3 has no intrinsic signaling properties (14). Upon NRG-1 binding, HER3 heterodimerizes with HER2, resulting in activation of the HER2 tyrosine kinase domain, HER2 autophosphorylation, and initiation of downstream intracellular signaling cascades (13). NRG-1 is expressed in bronchial epithelial cells (13,15,16) and is shed from the cell ...

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“…CuFi cells were used to generate polarized human CF airway epithelia as previously described (33). In brief, CuFi cells were cultured on collagen-coated plastic cell culture plates using bronchial epithelial growth medium (BEGM) consisting of a 1:1 mixture of Ham's F-12 and DMEM media supplemented with antibiotics and BEGM SingleQuots (Lonza, Basel Switzerland).…”

Section: Generation Of Recombinant Dna Constructs and Adenoviralmentioning

confidence: 99%

Comparative Processing and Function of Human and Ferret Cystic Fibrosis Transmembrane Conductance Regulator

Fisher

Liu

Yan

et al. 2012

Journal of Biological Chemistry

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Background: Species-specific differences in WT-and ⌬F508-CFTR biology exist. Results: Ferret WT-CFTR displays enhanced maturation efficiency and post-Golgi stability relative to human. Ferret ⌬F508-CFTR maturation was greater than human in certain cell lines; both orthologs lacked function in airway epithelia. Conclusion: Ferret and human CFTR have unique differences in processing and stability. Significance: Generation of a ⌬F508-CFTR ferret animal model may be useful.

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Development of cystic fibrosis and noncystic fibrosis airway cell lines

Cited by 162 publications

References 56 publications

Pharmacological Modulators of Sphingolipid Metabolism for the Treatment of Cystic Fibrosis Lung Inflammation

Pharmacological Modulators of Sphingolipid Metabolism for the Treatment of Cystic Fibrosis Lung Inflammation

Neuregulin-1-Human Epidermal Receptor-2 Signaling Is a Central Regulator of Pulmonary Epithelial Permeability and Acute Lung Injury

Comparative Processing and Function of Human and Ferret Cystic Fibrosis Transmembrane Conductance Regulator

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