scholarly journals circRNA expression profiling of colon tissue from mesalazine-treated mouse of inflammatory bowel disease reveals an important circRNA-miRNA-mRNA pathway

Aging ◽  
2021 ◽  
Author(s):  
Wei Zhou ◽  
Haiyin Zhang ◽  
Yibin Pan ◽  
Yanwu Xu ◽  
Yongqing Cao
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Expression Profiling ◽  
Treated Mouse ◽  
Colon Tissue ◽  
Inflammatory Bowel

Importance of TLR9-IL23-IL17 axis in inflammatory bowel disease development: Gene expression profiling study

2018 ◽  
Vol 197 ◽  
pp. 86-95 ◽  
Author(s):  
Sanja Dragasevic ◽  
Biljana Stankovic ◽  
Aleksandra Sokic-Milutinovic ◽  
Tomica Milosavljevic ◽  
Tamara Milovanovic ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Bowel Disease ◽  
Gene Expression Profiling ◽  
Bowel Disease ◽  
Expression Profiling ◽  
Disease Development ◽  
Inflammatory Bowel

scholarly journals Identification of Novel Predictor Classifiers for Inflammatory Bowel Disease by Gene Expression Profiling

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e76235 ◽  
Author(s):  
Trinidad Montero-Meléndez ◽  
Xavier Llor ◽  
Esther García-Planella ◽  
Mauro Perretti ◽  
Antonio Suárez
Keyword(s):  
Gene Expression ◽  
Inflammatory Bowel Disease ◽  
Gene Expression Profiling ◽  
Bowel Disease ◽  
Expression Profiling ◽  
Inflammatory Bowel

scholarly journals A4 THE CIRCADIAN TIMING OF INFLAMMATORY BOWEL DISEASE

2021 ◽  
Vol 4 (Supplement_1) ◽  
pp. 4-5
Author(s):  
Z Taleb ◽  
K Stokes ◽  
H Wang ◽  
S M Collins ◽  
W I Khan ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Circadian Clock ◽  
Bowel Disease ◽  
Mutant Mice ◽  
Intestinal Epithelial ◽  
Wild Type ◽  
Colon Tissue ◽  
Rhythmic Expression ◽  
Inflammatory Bowel

Abstract Background The circadian clock is a highly conserved molecular pacemaker found in nearly every cell of the body. It consists of the genes BMAL1 and CLOCK that positively regulate CRY and PER, their negative regulators, resulting in a transcription/translation feedback loop that has a 24 hour cycle. This core clock mechanism drives the rhythmic expression of over 40% of the genome in a tissue-specific manner and therefore imposes 24 hour rhythms on many physiological processes. Shift work, which causes disruptions to the natural 24 hour physiological rhythms, has been shown to lead to an increased incidence of inflammatory bowel disease (IBD). Aims This study aims to characterize daily rhythms in inflammation and regeneration of the colon upon induction of acute colitis. We also aim to investigate the intestinal epithelial-specific effects of circadian clock disruption on overall disease progression. We hypothesize that the absence of a functional circadian clock eliminates proliferation rhythms of intestinal epithelial cells and disrupts the rhythms of inflammatory cytokines, thereby increasing the pathogenesis of IBD. Methods We tested the role of the clock in IBD using BMAL1+/+ (wild type) and BMAL1-/- (null mutant) mice. We also investigated the effects of the circadian clock specific to intestinal epithelial tissue using Vil+/+;BMAL1flox/flox (control) and VilCre/+;BMAL1flox/flox (conditional intestinal epithelial mutant) mice. Dextran Sulfate Sodium (DSS) was applied to induce acute colitis. Results We observed significantly decreased survival of BMAL1 circadian clock mutant mice when given colitis. A histology analysis indicates increased lesioning and overall inflammation in BMAL1-/- colon tissue. Disease activity and cytokine analyses reveal time-dependent severity in inflammatory response that is worse in BMAL1-/- mice. To test the circadian rhythms in intestinal regeneration of mice with IBD, we performed a 24 hour analysis comparing epithelial cell proliferation and cell death in colon tissue. We observed rhythmic expression of phosphor-histone H3 (a mitosis marker) in wild type mice which is eliminated in the BMAL1-/- lacking a circadian clock. Cell death which was measured by caspase 3 did not exhibit any differences between genotypes. Based on these results, we conclude that the loss of clock function leads to impaired regeneration during IBD, in part due to decreased and arrhythmic cell proliferation. Preliminary results in our VilCre/+;BMAL1flox/flox conditional intestinal epithelial mutant mice indicate that some of these effects may be epithelial-specific. Conclusions Our results support a critical role of the circadian clock in inflammatory bowel disease development. These data highlight that the circadian clock affects the regenerative abilities of intestinal epithelial cells. Funding Agencies CIHRChron’s and Colitis Canada, Ontario, University of Windsor

P142 TARGETED COLON DELIVERY OF NIPEP-IM-0127 PEPTIDE FOR INFLAMMATORY BOWEL DISEASE (IBD) TREATMENT

2020 ◽  
Vol 26 (Supplement_1) ◽  
pp. S35-S35
Author(s):  
Deogil Kim ◽  
Dong Woo Lee ◽  
Beom Soo Jo ◽  
Yoon Shin Park ◽  
Jue Yeon Lee ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Complex Formation ◽  
Bowel Disease ◽  
Immune Modulation ◽  
Colon Tissue ◽  
Autoimmune Reaction ◽  
Mucosal Regeneration ◽  
Type Vii Collagen ◽  
Repeated Dose Toxicity ◽  
Inflammatory Bowel

Abstract Under Inflammatory bowel disease (IBD), autoantibody-type VII collagen complex can induce autoimmune reaction and continue with the inflammation. Here, we introduced synthetic 19 amino acid sequenced peptide termed as NIPEP-IM-0127 that inhibits autoantibody-type VII collagen complex formation. The NIPEP-IM-0127 was further formulated for oral administration. Primary function of NIPEP-IM-0127 selectively localizes to wound gut barrier and masks exposed type VII collagen, which is the starting of autoimmune reaction. Disrupted type VII collagen by the disease was bound to the applied peptide, which interfere autoimmune complex formation by competitive binding inhibition between antibody and peptide. NIPEP-IM-0127 thus recovered inflammatory cytokine level by the inhibition of immune complex creation. The orally applied NIPEP-IM-0127 peptide was primarily detected at the surface of colon tissue after 9 hours of administration, while no distributions were shown in other organs. Most importantly, significant mucosal regeneration and healing has been achieved by NIPEP-IM-0127. The following GLP toxicity studies, including safety pharmacology, genotoxicity, single and repeated dose toxicity, demonstrated that NIPEP-IM-0127 showed no significant toxic effect in in mouse and monkey. Taken together, the NIPEP-IM-0127 is suggested to be a novel therapeutic candidate for IBD treatment by the dual effects combining immune modulation and intestine barrier healing.

scholarly journals Mechanism and therapeutic effect of umbilical cord mesenchymal stem cells in inflammatory bowel disease

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Xing-hua Pan ◽  
Qing-qing Li ◽  
Xiang-qing Zhu ◽  
Zi-an Li ◽  
Xue-min Cai ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Umbilical Cord ◽  
Normal Control ◽  
Bowel Disease ◽  
Therapeutic Effects ◽  
Colon Tissue ◽  
Junction Protein ◽  
Inflammatory Bowel

AbstractInflammatory bowel disease (IBD) is a persistent and chronic disease that is characterized by destructive gastrointestinal (GI) inflammation. Researchers are trying to identify and develop new and more effective treatments with no side effects. Acute and chronic mouse models of IBD were established using dextran sulfate sodium (DSS) solution. To evaluate the efficacy and mechanism, umbilical cord mesenchymal stem cells (UCMSCs) were obtained from Kunming (KM) mice and humans. In the chronic IBD study, the survival rates of the normal control, model, mouse UCMSC (mUCMSC) and human UCMSC (hUCMSC) groups were 100%, 40%, 86.7%, and 100%, respectively. The histopathological scores of the normal control, intraperitoneal injection, intravenous treatment, and model groups were 0.5 ± 0.30, 5.9 ± 1.10, 8.7 ± 1.39, and 8.8 ± 1.33 (p = 0.021). UCMSCs promoted the expression of the intestinal tight junction protein occludin, downregulated the protein expression of the autophagy marker LC3A/B in colon tissue, and upregulated the expression of VEGF-A and VEGFR-1 at the injured site. This study provides an experimental model for elucidating the therapeutic effects of UCMSCs in IBD. We provide a theoretical basis and method for the clinical treatment of IBD using UCMSCs.

scholarly journals High-Resolution Gene Expression Profiling Using RNA Sequencing in Patients With Inflammatory Bowel Disease and in Mouse Models of Colitis

2015 ◽  
Vol 9 (6) ◽  
pp. 492-506 ◽  
Author(s):  
Kristine Holgersen ◽  
Burak Kutlu ◽  
Brian Fox ◽  
Kyle Serikawa ◽  
James Lord ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Bowel Disease ◽  
High Resolution ◽  
Gene Expression Profiling ◽  
Rna Sequencing ◽  
Mouse Models ◽  
Bowel Disease ◽  
Expression Profiling ◽  
Inflammatory Bowel

5-Lipoxygenase-derived lipid mediators are not required for the development of NSAID-induced inflammatory bowel disease in IL-10−/−mice

2008 ◽  
Vol 294 (2) ◽  
pp. G477-G488 ◽  
Author(s):  
Seiko Narushima ◽  
Daniel DiMeo ◽  
Jun Tian ◽  
Juan Zhang ◽  
Dahzi Liu ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
Bowel Disease ◽  
Early Time ◽  
Neutrophil Infiltration ◽  
Lipid Mediators ◽  
Colon Tissue ◽  
Nsaid Treatment ◽  
Inflammatory Bowel ◽  
Ifn Γ

Leukotrienes are potent lipid mediators derived from the metabolism of arachidonic acid by the enzyme 5-lipoxygenase (5-LO). Elevated levels of the proinflammatory leukotriene LTB4have been found in preclinical models of inflammatory bowel disease (IBD) as well as in colon tissue from individuals with IBD. We therefore determined the extent to which absence of 5-LO-derived lipid mediators would alter the colitis in IL-10−/−mice, a model of human IBD. IL-10−/−/5-LO−/−mice were generated and were healthy. Absence of 5-LO did not alter the development of spontaneous colitis in IL-10-deficient mice. We then evaluated the extent to which absence of 5-LO would alter the development of NSAID-induced colitis in IL-10−/−mice. Absence of 5-LO did not delay the onset or alter the severity of inflammation in NSAID-treated IL-10−/−mice. At an early time point, 3 days after NSAID treatment was initiated, a qualitative increase in the number of dendritic cells and CD4+T cells was noted in the colons of IL-10−/−/5-LO−/−; however, this difference was no longer present after 14 days of NSAID treatment. Absence of 5-LO did not alter the degree of neutrophil infiltration into the in this model. Absence of 5-LO does not alter the development of IFN-γ producing Th1-type CD4+T cells or IL-17 producing CD4+T cells. Absence of 5-LO-derived mediators did not alter the expression of the adhesion molecules ICAM-1 and P-selectin. Development of colitis in IL-10−/−mice was associated with increased levels of the 5-LO-derived anti-inflammatory lipoxin LXA4. These studies demonstrate that 5-LO-derived leukotrienes are not required for the development or maintenance of spontaneous or NSAID-induced colonic inflammation in IL-10−/−mice.

scholarly journals Treatment of Inflammatory Bowel Disease Associated E. coli with Ciprofloxacin and E. coli Nissle in the Streptomycin-Treated Mouse Intestine

PLoS ONE ◽  
2011 ◽  
Vol 6 (8) ◽  
pp. e22823 ◽  
Author(s):  
Andreas Munk Petersen ◽  
Susanne Schjørring ◽  
Sarah Choi Gerstrøm ◽  
Karen Angeliki Krogfelt
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Treated Mouse ◽  
E Coli ◽  
Mouse Intestine ◽  
Inflammatory Bowel
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