Saccharomyces boulardii has no effect on cholera toxin-induced water and electrolyte secretion in the human jejunum

1995 ◽  
Vol 108 (4) ◽  
pp. A290
1997 ◽  
Vol 9 (9) ◽  
pp. 887-891 ◽  
Author(s):  
Thomas A. Hinterleitner ◽  
Wolfgang Petritsch ◽  
Gudrun Dimsity ◽  
Hugues Berard ◽  
J.-M. Lecomte ◽  
...  

1998 ◽  
Vol 64 (2) ◽  
pp. 564-568 ◽  
Author(s):  
Rogelio L. Brandão ◽  
Ieso M. Castro ◽  
Eduardo A. Bambirra ◽  
Sheila C. Amaral ◽  
Luciano G. Fietto ◽  
...  

ABSTRACT As is the case for Saccharomyces boulardii, Saccharomyces cerevisiae W303 protects Fisher rats against cholera toxin (CT). The addition of glucose or dinitrophenol to cells of S. boulardii grown on a nonfermentable carbon source activated trehalase in a manner similar to that observed for S. cerevisiae. The addition of CT to the same cells also resulted in trehalase activation. Experiments performed separately on the A and B subunits of CT showed that both are necessary for activation. Similarly, the addition of CT but not of its separate subunits led to a cyclic AMP (cAMP) signal in both S. boulardii and S. cerevisiae. These data suggest that trehalase stimulation by CT probably occurred through the cAMP-mediated protein phosphorylation cascade. The requirement of CT subunit B for both the cAMP signal and trehalase activation indicates the presence of a specific receptor on the yeasts able to bind to the toxin, a situation similar to that observed for mammalian cells. This hypothesis was reinforced by experiments with 125I-labeled CT showing specific binding of the toxin to yeast cells. The adhesion of CT to a receptor on the yeast surface through the B subunit and internalization of the A subunit (necessary for the cAMP signal and trehalase activation) could be one more mechanism explaining protection against the toxin observed for rats treated with yeasts.


Gut ◽  
1988 ◽  
Vol 29 (10) ◽  
pp. 1337-1341 ◽  
Author(s):  
L K Munck ◽  
A Mertz-Nielsen ◽  
H Westh ◽  
K Bukhave ◽  
E Beubler ◽  
...  

1981 ◽  
Vol 241 (3) ◽  
pp. G248-G252 ◽  
Author(s):  
E. A. Swabb ◽  
Y. H. Tai ◽  
L. Jordan

The effect of luminal berberine hydrochloride concentration on cholera toxin-induced water and electrolyte secretion and on normal water and electrolyte transport was determined in vivo in the cannulated, perfused rat ileum using [14C]polyethylene glycol as a nonabsorbable marker. Berberine reduced the cholera toxin-induced secretion of water, Na, Cl, and calculated residual ion (primarily HCO3) in a concentration-dependent manner. The effect of berberine on cholera toxin-induced ileal secretion was evident 60-80 min after exposure and was reversed 60–80 min after removal of berberine from the perfusate. Mild changes in mucosal histology (villous tip edema) due to cholera toxin were also reversed by berberine. Berberine did not significantly alter normal ileal water and electrolyte transport.


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