Protection of gastric mucus gel layer from pepsininduced destruction by ecabet sodium, a novel locallyacting antiulcer agent. Analytical, histological and ultrastructural assessment

1998 ◽  
Vol 114 ◽  
pp. A178
Author(s):  
M. Kinoshita ◽  
M. Endo ◽  
A. Yasoshima ◽  
N. Saito ◽  
E. Kume ◽  
...  
1997 ◽  
Vol 73 ◽  
pp. 78
Author(s):  
Mine Kinpshita ◽  
Mika Endo ◽  
Akira Yasoshima ◽  
Susumu Chishima ◽  
Kazuva Yamasaki ◽  
...  

1997 ◽  
Vol 26 (suppl 3) ◽  
pp. P8-P8
Author(s):  
J Newton ◽  
N Jordan ◽  
G Williams ◽  
A Allen ◽  
O James ◽  
...  
Keyword(s):  

1992 ◽  
Vol 14 ◽  
pp. S82-S87 ◽  
Author(s):  
Lenard M. Lichtenberger ◽  
Tariq N. Ahmed ◽  
José C. Barreto ◽  
Ya-Chu Judy Kao ◽  
Elizabeth J. Dial
Keyword(s):  

1991 ◽  
Vol 26 (5) ◽  
pp. 582-587 ◽  
Author(s):  
Yuichi Komuro ◽  
Kazuhiko Ishihara ◽  
Susumu Ohara ◽  
Katsunori Saigenji ◽  
Kyoko Hotta

1998 ◽  
Vol 114 ◽  
pp. A181
Author(s):  
H. Kodaira ◽  
M. Kagoshima ◽  
E. Nogami ◽  
K. Ishii

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Helen Earley ◽  
Grainne Lennon ◽  
J. Calvin Coffey ◽  
Desmond C. Winter ◽  
P. Ronan O’Connell

AbstractButyrate is the primary energy source for colonocytes and is essential for mucosal integrity and repair. Butyrate deficiency as a result of colonic dysbiosis is a putative factor in ulcerative colitis (UC). Commensal microbes are butyrogenic, while others may inhibit butyrate, through hydrogenotropic activity. The aim of this study was to quantify butyrogenic and hydrogenotropic species and determine their relationship with inflammation within the colonic mucus gel layer (MGL). Mucosal brushings were obtained from 20 healthy controls (HC), 20 patients with active colitis (AC) and 14 with quiescent colitis (QUC). Abundance of each species was determined by RT-PCR. Inflammatory scores were available for each patient. Statistical analyses were performed using Mann–Whitney-U and Kruskall-Wallis tests. Butyrogenic R. hominis was more abundant in health than UC (p < 0.005), prior to normalisation against total bacteria. Hydrogenotropic B. wadsworthia was reduced in AC compared to HC and QUC (p < 0.005). An inverse correlation existed between inflammation and R. hominis (ρ − 0.460, p < 0.005) and B. wadsworthia (ρ − 0.646, p < 0.005). Other hydrogenotropic species did not widely colonise the MGL. These data support a role for butyrogenic bacteria in UC. Butyrate deficiency in UC may be related to reduced microbial production, rather than inhibition by microbial by-products.


2005 ◽  
Vol 51 (4) ◽  
pp. 287-291 ◽  
Author(s):  
Akira SHIMOTOYODOME ◽  
Shinichi MEGUO ◽  
Ichiro TOKIMITSU ◽  
Takashi SAKATA
Keyword(s):  

2020 ◽  
Author(s):  
Helen Earley ◽  
Grainne Lennon ◽  
Desmond Winter ◽  
Calvin Coffey ◽  
Ronan O'Connell

Abstract Butyrate is the primary energy source for colonocytes and is essential for mucosal integrity and repair. Butyrate deficiency as a result of colonic dysbiosis is a putative factor in ulcerative colitis (UC). Commensal microbes are butyrogenic, while others have an inhibitory effect, through hydrogenotropic activity. The aim of this study was to quantify butyrogenic and hydrogenotropic species and determine their relationship with inflammation within the colonic mucus gel layer (MGL).Mucosal brushings were obtained from 20 patients with active colitis (AC), 20 healthy controls (HC) and 14 with quiescent colitis (QUC). Abundance of each species was determined by RT-PCR. Inflammatory scores were available for each patient. Statistical analyses were performed using Mann-Whitney-U and Kruskall-Wallis tests.Butyrogenic R. hominis was more abundant in health than UC (p<0.005). Hydrogenotropic B. wadsworthia was reduced in AC compared to HC and QUC (p<0.005). An inverse correlation existed between inflammation and R. hominis (ρ -0.460, p >0.005) and B. wadsworthia (ρ -0.646, p >0.005). Other hydrogenotropic species did not widely colonise the MGL. These data support a role for butyrogenic and some species of hydrogenotropic bacteria in UC. Butyrate deficiency in UC may be related to reduced microbial production, rather than inhibition by microbial by-products.


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