scholarly journals Intrarectal administration of mCRAMP-encoding plasmid reverses exacerbated colitis in Cnlp−/− mice

Gene Therapy ◽  
2012 ◽  
Vol 20 (2) ◽  
pp. 187-193 ◽  
Author(s):  
E K K Tai ◽  
W K K Wu ◽  
X J Wang ◽  
H P S Wong ◽  
L Yu ◽  
...  
2004 ◽  
Vol 180 (9) ◽  
pp. 557-562 ◽  
Author(s):  
Vassilis E. Kouloulias ◽  
John R. Kouvaris ◽  
George Pissakas ◽  
John D. Kokakis ◽  
Christos Antypas ◽  
...  

1994 ◽  
Vol 266 (5) ◽  
pp. R1659-R1663 ◽  
Author(s):  
K. J. McHugh ◽  
S. M. Collins ◽  
H. P. Weingarten

Experimental colitis, induced in rats by intrarectal administration of trinitrobenzenesulfonic acid (TNB), results in a suppression of eating for 3 days. Because interleukin-1 (IL-1) is elevated within 24 h after TNB treatment, and because chronic administration of IL-1 leads to a pattern of anorexia similar to that seen after TNB, we evaluated the role of endogenous IL-1 in the anorexia observed in the TNB model. Human recombinant IL-1 receptor antagonist (rhIL-1ra) was administered chronically via osmotic minipump either peripherally or centrally after TNB treatment. Peripheral delivery of 40 micrograms/h rhIL-1ra significantly attenuated TNB-induced anorexia. However, 24 micrograms/h rhIL-1ra attenuated TNB-induced anorexia only when delivered centrally, not peripherally. These findings implicate central IL-1 receptors in the suppression of eating during acute experimental colitis but leave open a possible involvement of peripheral IL-1 receptors.


1980 ◽  
Vol 10 (2) ◽  
pp. 105-109
Author(s):  
Shinsuke Watanabe ◽  
Bunzo Nishioka ◽  
Yoshihiro Fujita ◽  
Takashi Ueda ◽  
Osamu Kojima ◽  
...  

1993 ◽  
Vol 264 (5) ◽  
pp. R871-R876 ◽  
Author(s):  
K. J. McHugh ◽  
H. P. Weingarten ◽  
C. Keenan ◽  
J. L. Wallace ◽  
S. M. Collins

We measured daily food intake and body weight in rats before and after the induction of colitis by intrarectal administration of either 2,4,6-trinitrobenzenesulfonic acid in ethyl alcohol (TNBE) or 4% acetic acid (AA). Administration of TNBE or AA induced inflammation in the distal colon, which was reflected by a significant increase in myeloperoxidase (MPO) activity in the colon. On days 1, 2, and 3 after induction of colitis by TNBE, food intake fell by 80, 70, and 50%, respectively, compared with pretreatment values; food intake returned to normal by day 4. Body weight fell within 24 h after induction of colitis and remained 10% less than control for at least 5 days. Colitis induced by AA produced a similar pattern and degree of decreased food intake and weight loss. Treatment with the 5'-lipoxygenase inhibitor MK-886 significantly reduced concentrations of leukotriene B4 in the colon of TNBE-treated rats but did not affect food intake. In contrast, the cyclooxygenase inhibitor indomethacin decreased prostaglandin E2 concentrations in the colon but also attenuated the suppression of feeding by 52 and 64% on the first 2 days after induction of colitis by TNBE. These results identify a specific prostaglandin-mediated suppression of feeding in the rat with acute colitis induced by TNBE and illustrate the utility of this model for studying mechanisms underlying anorexia associated with inflammation of the gastrointestinal tract.


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