scholarly journals Microbiota and mucosal defense in IBD: an update

2019 ◽  
Vol 13 (10) ◽  
pp. 963-976 ◽  
Author(s):  
Eduard F. Stange ◽  
Bjoern O. Schroeder
Keyword(s):  
2013 ◽  
Vol 144 (7) ◽  
pp. 1466-1477.e9 ◽  
Author(s):  
Bryan E. Essien ◽  
Helmut Grasberger ◽  
Rachael D. Romain ◽  
David J. Law ◽  
Natalia A. Veniaminova ◽  
...  

BIOCELL ◽  
2003 ◽  
Vol 27 (2) ◽  
pp. 163-172 ◽  
Author(s):  
Alicia B. Penissi ◽  
Mar韆 I. Rudolph ◽  
Ram髇 S. Piezzi
Keyword(s):  

2011 ◽  
Vol 6 (6) ◽  
pp. 426-438 ◽  
Author(s):  
M.A. Abd El-Kader ◽  
M.M. Ali ◽  
N.M. El-Sammad ◽  
M.A. El-Shaer

2005 ◽  
Vol 145 (3) ◽  
pp. 275-282 ◽  
Author(s):  
John L Wallace ◽  
Pallavi R Devchand

2008 ◽  
Vol 134 (4) ◽  
pp. A-655
Author(s):  
Atsuhiro Masuda ◽  
Masaru Yoshida ◽  
Tsukasa Ishida ◽  
Ryo Chinzei ◽  
Hiroshi Tanaka ◽  
...  

1983 ◽  
Vol 50 (3) ◽  
pp. 311-317
Author(s):  
S. C. Sanyal

2003 ◽  
Vol 284 (3) ◽  
pp. G399-G410 ◽  
Author(s):  
Sonlee D. West ◽  
Kenneth S. Helmer ◽  
Lily K. Chang ◽  
Yan Cui ◽  
George H. Greeley ◽  
...  

This study was done to examine the role of CCK in gastric mucosal defense and to assess the gastroprotective roles of nitric oxide and blood flow. In rats, the CCK secretagogues oleate and soybean trypsin inhibitor augmented gastric mucosal blood flow and prevented gastric injury from luminal irritants. Type A CCK receptor blockade negated CCK secretagogue-induced gastroprotection and exacerbated gastric injury from bile and ethanol but did not block adaptive cytoprotection. CCK secretagogue-induced gastroprotection and hyperemia were negated by nonselective nitric oxide synthase (NOS) inhibition ( N G-nitro-l-arginine methyl ester) but not by selective inducible NOS inhibition (aminoguanidine). Gastric mucosal calcium-dependent NOS activity, but not calcium-independent NOS activity, was increased following CCK and CCK secretagogues. The release of endogenous CCK plays a role in the intrinsic gastric mucosal defense system against injury from luminal irritants. The protective mechanism appears to involve increased production of nitric oxide from primarily the constitutive isoforms of NOS and a resultant increase in blood flow.


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