Methylated β-Cyclodextrins: Influence of Degree and Pattern of Substitution on the Thermodynamics of Complexation with Tauro- and Glyco-Conjugated Bile Salts

Langmuir ◽  
2011 ◽  
Vol 27 (10) ◽  
pp. 5832-5841 ◽  
Author(s):  
Christian Schönbeck ◽  
Peter Westh ◽  
Jens Christian Madsen ◽  
Kim Lambertsen Larsen ◽  
Lars Wagner Städe ◽  
...  
2010 ◽  
Vol 69 (1-2) ◽  
pp. 201-211 ◽  
Author(s):  
René Holm ◽  
Jens Christian Madsen ◽  
Wei Shi ◽  
Kim Lambertsen Larsen ◽  
Lars Wagner Städe ◽  
...  

1985 ◽  
Vol 69 (s12) ◽  
pp. 10P-10P
Author(s):  
C.O. Mills ◽  
S. Iqbal ◽  
E. Elias

2000 ◽  
Vol 63 (10) ◽  
pp. 1369-1376 ◽  
Author(s):  
WILLIAM P. CHARTERIS ◽  
PHILLIP M. KELLY ◽  
LORENZO MORELLI ◽  
J. KEVIN COLLINS

Virtually every antibiotic may cause in vivo alterations in the number, level, and composition of the indigenous microbiotae. The degree to which the microbiotae are disturbed depends on many factors. Although bile may augment antibiotic activity, studies on the effect of bile on the antibiotic susceptibility of indigenous and exogenous probiotic microorganisms are lacking. It was against this background that the antibiotic susceptibility of 37 bile salt–tolerant Lactobacillus and 11 Bifidobacterium isolates from human and other sources was determined in the presence of 0.5% wt/wt oxgall (conjugated bile salts). Oxgall did not affect the intrinsic resistance of lactobacilli to metronidazole (5 μg), vancomycin (30 μg), and cotrimoxazole (25 μg), whereas it resulted in a complete loss of resistance to polymyxin B (300 μg) and the aminoglycosides gentamicin (10 μg), kanamycin (30 μg), and streptomycin (10 μg) for most strains studied (P < 0.001). Oxgall did not affect the intrinsic resistance of bifidobacteria to metronidazole and vancomycin, whereas polymyxin B and co-trimoxazole resistance was diminished (P < 0.05) and aminoglycoside resistance was lost (P < 0.001). Seven lactobacilli, but no bifidobacteria strain, showed unaltered intrinsic antibiotic resistance profiles in the presence of oxgall. Oxgall affected the extrinsic susceptibility of lactobacilli and bifidobacteria to penicillin G (10 μg), ampicillin (10 μg), tetracycline (30 μg), chloramphenicol (30 μg), erythromycin (15 μg), and rifampicin (5 μg) in a source- and strain-dependent manner. Human strain–drug combinations of lactobacilli (P < 0.05) and bifidobacteria (P < 0.01) were more likely to show no change or decreased susceptibility compared with other strain-drug combinations. The antimicrobial activity spectra of polymyxin B and the aminoglycosides should not be considered limited to gram-negative bacteria but extended to include gram-positive genera of the indigenous and transiting microbiotae in the presence of conjugated bile salts. Those lactobacilli (7 of 37) that show unaltered intrinsic and diminished extrinsic antibiotic susceptibility in the presence of oxgall may possess greater upper gastrointestinal tract transit tolerance in the presence of antibiotics.


1986 ◽  
Vol 251 (5) ◽  
pp. G688-G694
Author(s):  
J. L. Goldstein ◽  
L. N. Schmidt ◽  
F. J. Al-Bazzaz ◽  
T. J. Layden

Bile salts have been implicated as a cause of esophageal injury. We examined in vitro the changes in ionic transport of the rabbit esophagus resulting from taurine-conjugated bile salts at neutral pH to define and characterize their actions independent of hydrogen ion. In an Ussing chamber changes in potential difference (PD, mV), short-circuit current (SCC, microA X cm-2) and resistance (R, omega X cm2) resulting from taurocholate (TC), taurodeoxycholate (TDC) and taurochenodeoxycholate (TCDC) were studied. Transport properties were unaffected by TC at 5 and 10 mM. With TDC (5 mM) there was an initial rise in SCC and PD. After 60 min PD and R declined in association with an increase in paracellular permeability as measured by [14C]sucrose flux. TCDC (5.0 and 7.5 mM) caused a sustained rise in PD and SCC with a greater rise seen at 7.5 mM. The rise in SCC after TCDC was secondary to an increase in net sodium absorption as basal net sodium absorption increased threefold from 0.15 +/- 0.03 to 0.44 +/- 0.10 mu eq X cm-2 X h-1. Increased net sodium absorption accounted for 73% of the TCDC-induced rise in SCC. Amiloride (10(-4) M) added to the mucosal solution significantly inhibited this bile salt-induced rise in SCC. We conclude that bile salts alter ionic transport in the esophageal mucosa independent of hydrogen ion. These changes are characterized by an early selective increase in apical membrane cation conductance and with longer exposure, particularly in the presence of more hydrophobic bile salts, there is a marked increase in paracellular conductance.


2005 ◽  
Vol 46 (11) ◽  
pp. 2325-2338 ◽  
Author(s):  
G. Pütz ◽  
W. Schmider ◽  
R. Nitschke ◽  
G. Kurz ◽  
H. E. Blum

1972 ◽  
Vol 139 (1) ◽  
pp. 70-73 ◽  
Author(s):  
D. A. Cook ◽  
L. M. Hagerman ◽  
D. L. Schneider

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