Comparison of Human Tracheal/Bronchial Epithelial Cell Culture and Bovine Nasal Respiratory Explants for Nasal Drug Transport Studies

2005 ◽  
Vol 94 (9) ◽  
pp. 1976-1985 ◽  
Author(s):  
Nagendra V. Chemuturi ◽  
Patrick Hayden ◽  
Mitch Klausner ◽  
Maureen D. Donovan
Keyword(s):  
Cell Culture ◽  
Epithelial Cell ◽  
Drug Transport ◽  
Bronchial Epithelial Cell ◽  
Epithelial Cell Culture ◽  
Bronchial Epithelial ◽  
Transport Studies

scholarly journals Evaluation of Differentiated Human Bronchial Epithelial Cell Culture Systems for Asthma Research

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Ceri E. Stewart ◽  
Elizabeth E. Torr ◽  
Nur H. Mohd Jamili ◽  
Cynthia Bosquillon ◽  
Ian Sayers
Keyword(s):  
Cell Culture ◽  
Epithelial Cell ◽  
Bronchial Epithelial Cell ◽  
Confocal Imaging ◽  
Primary Cells ◽  
Epithelial Cell Culture ◽  
Bronchial Epithelial ◽  
Culture Systems ◽  
Cell Culture Systems ◽  
E Cadherin

The aim of the current study was to evaluate primary (human bronchial epithelial cells, HBEC) and non-primary (Calu-3, BEAS-2B, BEAS-2B R1) bronchial epithelial cell culture systems as air-liquid interface- (ALI-) differentiated models for asthma research. Ability to differentiate into goblet (MUC5AC+) and ciliated (β-Tubulin IV+) cells was evaluated by confocal imaging and qPCR. Expression of tight junction/adhesion proteins (ZO-1, E-Cadherin) and development of transepithelial electrical resistance (TEER) were assessed. Primary cells showed localised MUC5AC, β-Tubulin IV, ZO-1, and E-Cadherin and developed TEER with, however, a large degree of inter- and intradonor variation. Calu-3 cells developed a more reproducible TEER and a phenotype similar to primary cells although with diffuse β-Tubulin IV staining. BEAS-2B cells did not differentiate or develop tight junctions. These data highlight the challenges in working with primary cell models and the need for careful characterisation and selection of systems to answer specific research questions.

scholarly journals Effect of Vaccine-Elicited Antibodies on Colonization of Neisseria meningitidis Serogroup B and C Strains in a Human Bronchial Epithelial Cell Culture Model

2017 ◽  
Vol 24 (10) ◽  
Author(s):  
Vianca Vianzon ◽  
Beate Illek ◽  
Gregory R. Moe
Keyword(s):  
Cell Culture ◽  
Epithelial Cell ◽  
Capsular Polysaccharide ◽  
Bronchial Epithelial Cell ◽  
Human Bronchial Epithelial Cell ◽  
Cell Culture Model ◽  
Epithelial Cell Culture ◽  
Bronchial Epithelial ◽  
Conjugate Vaccines ◽  
Culture Model

ABSTRACT Capsular polysaccharide-protein conjugate vaccines protect individuals from invasive disease and decrease carriage, which reduces spread of the organism in the population. In contrast, antibodies elicited by plain polysaccharide or protein antigen-based meningococcal (Men) vaccines have little or no effect on decreasing carriage. In this study, we investigated the mechanism by which vaccine-induced human immunoglobulin G (IgG) antibodies affect colonization by meningococcal serogroup B (MenB) or C (MenC) strains using a human bronchial epithelial cell culture model (16HBE14o-). Fluorescence microscopy showed that bacteria colonizing the apical side of 16HBE14o- monolayers had decreased capsular polysaccharide on the bacterial surface that resulted from shedding the capsule and not decreased production of polysaccharide. Capsular polysaccharide shedding depended on the presence of 16HBE14o- cells and bacteria but not direct adherence of the bacteria to the cells. Treatment of bacteria and cells with postimmunization MenC-conjugate IgG or murine anti-MenB polysaccharide monoclonal antibodies (MAbs) inhibited capsule shedding, microcolony dispersal, and invasion of the 16HBE14o- cell monolayer. In contrast, the IgG responses elicited by immunization with MenC polysaccharide (PS), MenB outer membrane vesicle (OMV)-based, or factor H binding protein (FHbp)-based vaccines were not different than preimmune IgG or no-treatment response. The results provide new insights on the mechanism by which high-avidity anticapsular antibodies elicited by polysaccharide-conjugate vaccines affect meningococcal colonization. The data also suggest that any effect on colonization by IgG elicited by OMV- or FHbp-based vaccines may involve a different mechanism.

Primary bronchial epithelial cell culture from explanted cystic fibrosis lungs

2010 ◽  
Vol 36 (2) ◽  
pp. 101-110 ◽  
Author(s):  
Malcolm Brodlie ◽  
Michael C. McKean ◽  
Gail E. Johnson ◽  
John D. Perry ◽  
Audrey Nicholson ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Cell Culture ◽  
Epithelial Cell ◽  
Bronchial Epithelial Cell ◽  
Epithelial Cell Culture ◽  
Bronchial Epithelial ◽  
Primary Bronchial Epithelial Cell

scholarly journals Retinoic acid improves baseline barrier function and attenuates TNF-α-induced barrier leak in human bronchial epithelial cell culture model, 16HBE 14o-

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0242536
Author(s):  
Patrick J. Callaghan ◽  
Elizabeth Rybakovsky ◽  
Bryan Ferrick ◽  
Sunil Thomas ◽  
James M. Mullin
Keyword(s):  
Cell Culture ◽  
Retinoic Acid ◽  
Barrier Function ◽  
Bronchial Epithelial Cell ◽  
Cell Culture Model ◽  
Epithelial Cell Culture ◽  
Bronchial Epithelial ◽  
Culture Model ◽  
Tnf Α ◽  
Cell Layers

Retinoic acid (RA) has been shown to improve epithelial and endothelial barrier function and development and even suppress damage inflicted by inflammation on these barriers through regulating immune cell activity. This paper thus sought to determine whether RA could improve baseline barrier function and attenuate TNF-α-induced barrier leak in the human bronchial epithelial cell culture model, 16HBE14o- (16HBE). We show for the first time that RA increases baseline barrier function of these cell layers indicated by an 89% increase in transepithelial electrical resistance (TER) and 22% decrease in 14C-mannitol flux. A simultaneous, RA-induced 70% increase in claudin-4 attests to RA affecting the tight junctional (TJ) complex itself. RA was also effective in alleviating TNF-α-induced 16HBE barrier leak, attenuating 60% of the TNF-α-induced leak to 14C-mannitol and 80% of the leak to 14C-inulin. Interleukin-6-induced barrier leak was also reduced by RA. Treatment of 16HBE cell layers with TNF-α resulted in dramatic decrease in immunostaining for occludin and claudin-4, as well as a downward “band-shift” in occludin Western immunoblots. The presence of RA partially reversed TNF-α’s effects on these select TJ proteins. Lastly, RA completely abrogated the TNF-α-induced increase in ERK-1,2 phosphorylation without significantly decreasing the TNF-driven increase in total ERK-1,2. This study suggests RA could be effective as a prophylactic agent in minimizing airway barrier leak and as a therapeutic in preventing leak triggered by inflammatory cascades. Given the growing literature suggesting a “cytokine storm” may be related to COVID-19 morbidity, RA may be a useful adjuvant for use with anti-viral therapies.

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