Document Detail


Talniflumate increases survival in a cystic fibrosis mouse model of distal intestinal obstructive syndrome.
MedLine Citation:
PMID:  16354791     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intestinal disease in cystic fibrosis (CF) mice closely mirrors aspects of obstructive syndromes in CF patients. The pathogenesis involves accumulation of mucoid debris in the crypts that fuse with intestinal content to form obstructing mucofeculant impactions. Treatment involves modalities that increase the fluidity of the luminal content, such as osmotic laxatives and liquid diets. We investigated the effects of talniflumate (Lomucin, Genaera Corporation, Plymouth Meeting, PA), a compound that may be beneficial to treatment of CF intestinal disease based on three mechanisms of action: mucus synthesis inhibition by blockade of the murine calcium-activated chloride channel 3 (mCLCA3), nonsteroidal anti-inflammatory effects, and inhibition of Cl(-)/HCO (-)(3) exchanger(s) involved in intestinal NaCl absorption. Cohorts of CF mice were fed control diet or diets containing either talniflumate (0.4 mg/g chow) or ibuprofen (0.4 mg/g chow) for 21 days to assess survival. Talniflumate significantly increased CF mouse survival from 26 to 77%, whereas ibuprofen had no effect (22% survival). Oral talniflumate did not alter crypt goblet cell numbers or change intestinal expression of mCLCA3 but tended to decrease crypt mucoid impaction. Ussing chamber studies indicated that talniflumate slightly increased the basal short-circuit current of CF intestine, but the change was not sensitive to secretagogue stimulation or bumetanide inhibition. In contrast, intracellular pH measurements of intact intestinal villous epithelium indicated that talniflumate significantly inhibited apical membrane Cl(-)/HCO (-)(3) exchange by >50%. We conclude that oral talniflumate increases the survival of CF mice, possibly by the beneficial effects of decreasing small intestinal NaCl absorption through the inhibition of apical membrane Cl(-)/HCO (-)(3) exchanger(s).
Authors:
Nancy M Walker; Janet E Simpson; Roy C Levitt; Kathryn T Boyle; Lane L Clarke
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2005-12-14
Journal Detail:
Title:  The Journal of pharmacology and experimental therapeutics     Volume:  317     ISSN:  0022-3565     ISO Abbreviation:  J. Pharmacol. Exp. Ther.     Publication Date:  2006 Apr 
Date Detail:
Created Date:  2006-03-22     Completed Date:  2006-05-25     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376362     Medline TA:  J Pharmacol Exp Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  275-83     Citation Subset:  IM    
Affiliation:
Dalton Cardiovascular Research Center, University of Missouri, Columbia, 65211, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
Benzofurans / therapeutic use*
Cell Count
Chloride Channels / biosynthesis
Cystic Fibrosis / complications*,  genetics
Cystic Fibrosis Transmembrane Conductance Regulator / genetics
Disease Models, Animal
Hydrogen-Ion Concentration
Intestinal Mucosa / cytology,  drug effects,  metabolism
Intestinal Obstruction / drug therapy*,  etiology,  metabolism
Intestine, Small / cytology,  drug effects,  metabolism
Ion Transport / drug effects
Mice
Mucins / biosynthesis
Mucoproteins / biosynthesis
Mutation
Pyridines / therapeutic use*
Grant Support
ID/Acronym/Agency:
DK44816/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents, Non-Steroidal; 0/Benzofurans; 0/Chloride Channels; 0/Clca3 protein, mouse; 0/Mucins; 0/Mucoproteins; 0/Pyridines; 0/talniflumate; 126880-72-6/Cystic Fibrosis Transmembrane Conductance Regulator

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


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