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Intrarectal nitric oxide administration prevents cellular infiltration but not colonic injury during dextran sodium sulfate colitis

Joan Vermeiren UGent, Pieter Hindryckx UGent, Glynn Van Nieuwenhuyse UGent, Debby Laukens UGent, Martine De Vos UGent, Nico Boon UGent and Tom Vandewiele UGent (2012) DIGESTIVE DISEASES AND SCIENCES. 57(7). p.1832-1837
abstract
During inflammation in the gastrointestinal tract, the production of nitric oxide (NO) is mediated by the mucosal conversion of l-arginine. Recently, it was shown that the gut microbiota can also produce NO. The effect of gut luminal NO on inflammatory processes of an experimental colitis mice model was investigated by administrating NO directly to the colon, mimicking microbial NO production. Twenty-four mice received daily intrarectal treatment with a NO donor in 2 doses and 8 mice were treated with placebo. Starting 1 day later, 18 of these mice were fed ad libitum with 4% of dextran sodium sulfate (DSS) in their drinking water to induce colitis. At day 6, histopathology (both the inflammation and damage score), myeloperoxidase (MPO)-activity, colon length and colonic permeability were evaluated. Co-administration of NO during DSS exposure inhibited the induction of an increasing colonic MPO-activity. This protective effect of NO was confirmed by the histological inflammation score showing a similar trend. The colonic permeability was restored when very low levels of NO were administered to the DSS-mice. On the other hand, the colon length of the NO-treated DSS-mice was negatively correlated with the NO dose and the histological damage score was not improved. Our results indicate that intrarectal administration of NO has clear anti-inflammatory effects in experimental colitis, but does not prevent colonic damage. Therefore, NO-producing microorganisms in the gut lumen should be accounted as a modulating process during colitis.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
ULCERATIVE-COLITIS, SYNTHASE ACTIVITY, INFLAMMATORY-BOWEL-DISEASE, Nitrate, Epithelial damage, Intestinal permeability, Experimental murine colitis, Reactive nitrogen species, Inflammatory bowel diseases, INTESTINAL PERMEABILITY, CROHNS-DISEASE, RATS, NITRATE, ABSENCE, IMPACT
journal title
DIGESTIVE DISEASES AND SCIENCES
Dig. Dis. Sci.
volume
57
issue
7
pages
1832 - 1837
Web of Science type
Article
Web of Science id
000305746100015
JCR category
GASTROENTEROLOGY & HEPATOLOGY
JCR impact factor
2.26 (2012)
JCR rank
36/73 (2012)
JCR quartile
2 (2012)
ISSN
0163-2116
DOI
10.1007/s10620-012-2105-8
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2125918
handle
http://hdl.handle.net/1854/LU-2125918
date created
2012-05-31 18:44:49
date last changed
2013-02-26 11:06:38
@article{2125918,
  abstract     = {During inflammation in the gastrointestinal tract, the production of nitric oxide (NO) is mediated by the mucosal conversion of l-arginine. Recently, it was shown that the gut microbiota can also produce NO. 
The effect of gut luminal NO on inflammatory processes of an experimental colitis mice model was investigated by administrating NO directly to the colon, mimicking microbial NO production. 
Twenty-four mice received daily intrarectal treatment with a NO donor in 2 doses and 8 mice were treated with placebo. Starting 1 day later, 18 of these mice were fed ad libitum with 4\% of dextran sodium sulfate (DSS) in their drinking water to induce colitis. At day 6, histopathology (both the inflammation and damage score), myeloperoxidase (MPO)-activity, colon length and colonic permeability were evaluated. 
Co-administration of NO during DSS exposure inhibited the induction of an increasing colonic MPO-activity. This protective effect of NO was confirmed by the histological inflammation score showing a similar trend. The colonic permeability was restored when very low levels of NO were administered to the DSS-mice. On the other hand, the colon length of the NO-treated DSS-mice was negatively correlated with the NO dose and the histological damage score was not improved. 
Our results indicate that intrarectal administration of NO has clear anti-inflammatory effects in experimental colitis, but does not prevent colonic damage. Therefore, NO-producing microorganisms in the gut lumen should be accounted as a modulating process during colitis.},
  author       = {Vermeiren, Joan and Hindryckx, Pieter and Van Nieuwenhuyse, Glynn and Laukens, Debby and De Vos, Martine and Boon, Nico and Vandewiele, Tom},
  issn         = {0163-2116},
  journal      = {DIGESTIVE DISEASES AND SCIENCES},
  keyword      = {ULCERATIVE-COLITIS,SYNTHASE ACTIVITY,INFLAMMATORY-BOWEL-DISEASE,Nitrate,Epithelial damage,Intestinal permeability,Experimental murine colitis,Reactive nitrogen species,Inflammatory bowel diseases,INTESTINAL PERMEABILITY,CROHNS-DISEASE,RATS,NITRATE,ABSENCE,IMPACT},
  language     = {eng},
  number       = {7},
  pages        = {1832--1837},
  title        = {Intrarectal nitric oxide administration prevents cellular infiltration but not colonic injury during dextran sodium sulfate colitis},
  url          = {http://dx.doi.org/10.1007/s10620-012-2105-8},
  volume       = {57},
  year         = {2012},
}

Chicago
Vermeiren, Joan, PIETER HINDRYCKX, Glynn Van Nieuwenhuyse, Debby Laukens, Martine De Vos, Nico Boon, and Tom Vandewiele. 2012. “Intrarectal Nitric Oxide Administration Prevents Cellular Infiltration but Not Colonic Injury During Dextran Sodium Sulfate Colitis.” Digestive Diseases and Sciences 57 (7): 1832–1837.
APA
Vermeiren, J., HINDRYCKX, P., Van Nieuwenhuyse, G., Laukens, D., De Vos, M., Boon, N., & Vandewiele, T. (2012). Intrarectal nitric oxide administration prevents cellular infiltration but not colonic injury during dextran sodium sulfate colitis. DIGESTIVE DISEASES AND SCIENCES, 57(7), 1832–1837.
Vancouver
1.
Vermeiren J, HINDRYCKX P, Van Nieuwenhuyse G, Laukens D, De Vos M, Boon N, et al. Intrarectal nitric oxide administration prevents cellular infiltration but not colonic injury during dextran sodium sulfate colitis. DIGESTIVE DISEASES AND SCIENCES. 2012;57(7):1832–7.
MLA
Vermeiren, Joan, PIETER HINDRYCKX, Glynn Van Nieuwenhuyse, et al. “Intrarectal Nitric Oxide Administration Prevents Cellular Infiltration but Not Colonic Injury During Dextran Sodium Sulfate Colitis.” DIGESTIVE DISEASES AND SCIENCES 57.7 (2012): 1832–1837. Print.