scholarly journals Alterations of Colonic Contractility in an Interleukin-10 Knockout Mouse Model of Inflammatory Bowel Disease

2015 ◽  
Vol 21 (1) ◽  
pp. 051-061 ◽  
Author(s):  
Jae Hyung Park ◽  
Joong Goo Kwon ◽  
Sun Joo Kim ◽  
Dae Kyu Song ◽  
Seok Guen Lee ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Bowel Disease ◽  
Knockout Mouse ◽  
Interleukin 10 ◽  
Knockout Mouse Model ◽  
Inflammatory Bowel

scholarly journals Corrigendum: Alterations of Colonic Contractility in an Interleukin-10 Knockout Mouse Model of Inflammatory Bowel Disease

2015 ◽  
Vol 21 (2) ◽  
pp. 300-300
Author(s):  
Jae Hyung Park ◽  
Joong Goo Kwon ◽  
Sun Joo Kim ◽  
Dae Kyu Song ◽  
Seok Guen Lee ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Bowel Disease ◽  
Knockout Mouse ◽  
Interleukin 10 ◽  
Knockout Mouse Model ◽  
Inflammatory Bowel

scholarly journals Impaired Autophagy in Intestinal Epithelial Cells Alters Gut Microbiota and Host Immune Responses

2018 ◽  
Vol 84 (18) ◽  
Author(s):  
Lingyu Yang ◽  
Chao Liu ◽  
Wenjing Zhao ◽  
Chuan He ◽  
Jinmei Ding ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Gut Microbiota ◽  
Bowel Disease ◽  
Knockout Mouse ◽  
Content Type ◽  
Knockout Mouse Model ◽  
Akkermansia Muciniphila ◽  
Host Health ◽  
Inflammatory Bowel

ABSTRACTEstablishing and maintaining beneficial interactions between the host and associated gut microbiota are pivotal requirements for host health. Autophagy is an important catabolic recycling pathway that degrades long-lived proteins and some organelles by lysosome to maintain cellular homeostasis. Although impaired autophagy is thought to be closely correlated with Crohn's disease (CD), the functional role of autophagy in the maintenance of gut microbiota is poorly understood. As autophagy-related 5 (Atg5) is a key gene associated with the extension of the phagophoric membrane in autophagic vesicles, we established a gut-specificAtg5knockout mouse model, and we found that the disruption of autophagic flux in the intenstinal epithelium cells dramatically altered the composition of the gut microbiota and reduced alpha diversity. Microbial function prediction indicated that the pathway allocated for infectious diseases was enriched inAtg5−/−mice. “CandidatusArthromitus” and thePasteurellaceaefamily were increased inAtg5−/−mice, whereasAkkermansia muciniphilaand theLachnospiraceaefamily were reduced. Transcriptome analysis revealed that two key inflammatory bowel disease (IBD)-related transcription factors, RORC and TBX21, of host cells were upregulated inAtg5−/−mice, thus elevating the Muc2-related immunological response. The findings suggest that intestinal autophagy plays a vital role in modulating the diversity and composition of gut microbiota.IMPORTANCEThe homeostasis of host-microbiota interactions is of great importance to host health. Previous studies demonstrated that disruption of autophagy was linked to inflammatory bowel disease. However, the interaction mechanism of gut microbiota regulated by autophagy was obscure. In an intestinal epithelium-specific autophagy-related 5 (Atg5) knockout mouse model, we observed a significant alteration and decreased diversity in the gut microbiota ofAtg5-deficient mice compared with that of wild-type mice. Although the numbers of some organisms (e.g.,Akkermansia muciniphilaand members of theLachnospiraceaefamily) associated with the control of inflammation decreased, those of proinflammationory bacteria (e.g., “CandidatusArthromitus”) and potential pathogens (thePasteurellaceaefamily) increased inAtg5−/−mice. Differential gene expression analysis revealed that two key genes,RORCandTBX21, involved in inflammatory bowel disease were upregulated inAtg5−/−mice. Our study suggests thatAtg5deficiency results in an imbalance of the host-microbe interaction and deterioration of the gut microenvironment.

scholarly journals Metabolomic Profiles Are Gender, Disease and Time Specific in the Interleukin-10 Gene-Deficient Mouse Model of Inflammatory Bowel Disease

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e67654 ◽  
Author(s):  
Victor K. Tso ◽  
Beate C. Sydora ◽  
Rae R. Foshaug ◽  
Thomas A. Churchill ◽  
Jason Doyle ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Bowel Disease ◽  
Interleukin 10 ◽  
Deficient Mouse ◽  
Inflammatory Bowel ◽  
Time Specific ◽  
Gene Deficient Mouse

Association between polymorphisms in the promoter region of interleukin-10 and susceptibility to inflammatory bowel disease

2014 ◽  
Vol 41 (3) ◽  
pp. 1299-1310 ◽  
Author(s):  
Hongchao Lv ◽  
Yongshuai Jiang ◽  
Jin Li ◽  
Mingming Zhang ◽  
Zhenwei Shang ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Promoter Region ◽  
Interleukin 10 ◽  
Inflammatory Bowel

S1740 The Effects of Rapamycin in the TNBS Mouse Model of Inflammatory Bowel Disease

2008 ◽  
Vol 134 (4) ◽  
pp. A-260
Author(s):  
Gary C. Bruns ◽  
Dave Cody ◽  
Russell J. Sheldon ◽  
George Zhang
Keyword(s):  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Mouse model of ulcerative colitis using trinitrobenzene sulfonic acid

2015 ◽  
Vol 10 (4) ◽  
pp. 860
Author(s):  
Irfan Ahmad Rather ◽  
Vivek K. Bajpai ◽  
Nam Gyeong-Jun
Keyword(s):  
Ulcerative Colitis ◽  
Inflammatory Bowel Disease ◽  
Mouse Model ◽  
Bowel Disease ◽  
Sulfonic Acid ◽  
Intestinal Inflammation ◽  
Cost Effective ◽  
Trinitrobenzene Sulfonic Acid ◽  
Clinical Presentations ◽  
Inflammatory Bowel

<p>Animal model of intestinal inflammation is of paramount significance that aids in discerning the pathologies underlying ulcerative colitis and Crohn’s disease, the two clinical presentations of inflammatory bowel disease. The 2,4,6-trinitrobenzene sulfonic acid (TNBS) colitis model represents one such intestinal inflammation-prototype that is generated in susceptible strains of mice through intra-rectal instillation of compound TNBS. In this paper, we demonstrate the experimental induction of TNBS-mediated colitis in a susceptible strain of ICR mice. This can be done by the following steps: a) acclimation, b) induction and c) observation. TNBS-mouse model provides the information in shortest possible time and simultaneously represents a cost effective and highly reproducible model method of studying the pathogenesis of inflammatory bowel disease.</p><p><strong>Video Clips</strong></p><p><a href="https://youtube.com/v/6MsuIGzH3uA">Acclimation and induction of TNBS</a>:          4.5 min</p><p><a href="https://youtube.com/v/ya66SNwoVag">Observation and drug administration</a>:      1.5 min</p>

scholarly journals Characterisation of enterocolitis in the piroxicam-accelerated interleukin-10 knock out mouse — A model mimicking inflammatory bowel disease

2014 ◽  
Vol 8 (2) ◽  
pp. 147-160 ◽  
Author(s):  
Kristine Holgersen ◽  
Peter Helding Kvist ◽  
Helle Markholst ◽  
Axel Kornerup Hansen ◽  
Thomas Lindebo Holm
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Interleukin 10 ◽  
Knock Out ◽  
Inflammatory Bowel ◽  
Knock Out Mouse
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