Document Detail


Physiologic modulation of bronchial epithelial cell barrier function by polycationic exposure.
MedLine Citation:
PMID:  8049079     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Bronchial epithelial cells provide a functional barrier to the movement of water and solutes between the luminal and interstitial compartments of the lung. Barrier integrity can be compromised by a variety of factors, including polycationic proteins released by inflammatory cells. We investigated the characteristics of epithelial barrier function and its modulation by cationic stimuli in canine bronchial epithelial (CBE) cells grown in culture. Morphologic characteristics were examined, and barrier function was assessed by measurements of transepithelial mannitol flux (flux) and electrical resistance (RT) during a stable, 3- to 14-day culture period. CBE cultures exhibited progressive mucociliary differentiation and contained nonciliated, ciliated, and neutral and acidic mucin-secretory cells. The synthetic polycation, poly-L-lysine (PLL), from 2.5 to 10 micrograms/ml, caused dose-related increases in flux and decreases in RT that were not accompanied by detectable release of lactate dehydrogenase (LDH) or changes in histochemical appearance. The effect on RT spontaneously reversed over a 15-h recovery period. The action of PLL on flux was not attenuated by treatment of the cells to stabilize cytoskeletal contractile elements but was immediately attenuated by the addition of heparin to the challenged cells. These results indicate that modulation of the barrier integrity of bronchial epithelial cells by cationic proteins, such as those released by inflammatory cells, represents a physiologic process that may be regulated by endogenous anionic factors.
Authors:
X Y Yu; B H Schofield; T Croxton; N Takahashi; E W Gabrielson; E W Spannhake
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of respiratory cell and molecular biology     Volume:  11     ISSN:  1044-1549     ISO Abbreviation:  Am. J. Respir. Cell Mol. Biol.     Publication Date:  1994 Aug 
Date Detail:
Created Date:  1994-09-06     Completed Date:  1994-09-06     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8917225     Medline TA:  Am J Respir Cell Mol Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  188-98     Citation Subset:  IM    
Affiliation:
Department of Environmental Health Sciences, Johns Hopkins School of Hygiene and Public Health, Baltimore, Maryland 21205.
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Transport / drug effects
Bronchi / cytology,  drug effects,  physiology*
Cell Differentiation
Cell Division / drug effects
Cells, Cultured
Cytochalasin B / pharmacology
DNA / biosynthesis
Dogs
Dose-Response Relationship, Drug
Electric Conductivity
Epithelial Cells
Epithelium / drug effects,  physiology
Heparin / pharmacology
Kinetics
L-Lactate Dehydrogenase / analysis
Mannitol / metabolism
Phalloidine / pharmacology
Polylysine / pharmacology*
Thymidine / metabolism
Time Factors
Grant Support
ID/Acronym/Agency:
ES-03505/ES/NIEHS NIH HHS; ES-03819/ES/NIEHS NIH HHS; HL-30195/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
14930-96-2/Cytochalasin B; 17466-45-4/Phalloidine; 25104-18-1/Polylysine; 50-89-5/Thymidine; 69-65-8/Mannitol; 9005-49-6/Heparin; 9007-49-2/DNA; EC 1.1.1.27/L-Lactate Dehydrogenase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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