scholarly journals Glucocorticoids differentially regulate Na-bile acid cotransport in normal and chronically inflamed rabbit ileal villus cells

2010 ◽  
Vol 298 (5) ◽  
pp. G675-G682 ◽  
Author(s):  
Steven Coon ◽  
Ramesh Kekuda ◽  
Prosenjit Saha ◽  
Uma Sundaram
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Western Blot ◽  
Bowel Disease ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Kinetic Studies ◽  
Rabbit Ileum ◽  
Expression Levels ◽  
Inflammatory Bowel

Previous studies have demonstrated that apical Na-bile acid cotransport (ASBT) is inhibited during chronic ileitis by both a decrease in the affinity as well as a decrease in the number of cotransporters. Methylprednisolone (MP), a commonly used treatment for inflammatory bowel disease (IBD, e.g., Crohn's disease), has been shown to reverse the inhibition of several other Na-solute cotransporters during chronic enteritis. However, the effect of MP on ASBT in the chronically inflamed ileum is not known. MP stimulated ASBT in villus cells from the normal rabbit ileum by increasing the cotransporter expression without a change in the affinity of the cotransporter for bile acid. Western blot studies demonstrated an increase in cotransporter expression. MP reversed the inhibition of ASBT in villus cells from the chronically inflamed ileum. Kinetic studies demonstrated that the mechanism of MP-mediated reversal of ASBT inhibition was secondary to a restoration of both affinity as well as cotransporter numbers. Western blot analysis demonstrated restoration of cotransporter numbers after MP treatment of rabbits with chronic ileitis. Thus MP stimulates ASBT in the normal ileum by increasing cotransporter numbers. MP reverses the inhibition of ASBT during chronic ileitis. However, MP restores the diminished affinity as well as cotransporter expression levels during chronic ileitis. Thus MP differentially regulates ASBT in the normal and in the chronically inflamed ileum.

scholarly journals Expression of inflammatory mediators in biofilm samples and clinical association in inflammatory bowel disease patients—a preliminary study

2021 ◽  
Author(s):  
Mayte Buchbender ◽  
Jakob Fehlhofer ◽  
Peter Proff ◽  
Tobias Möst ◽  
Jutta Ries ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Inflammatory Bowel Disease ◽  
Oral Cavity ◽  
Bowel Disease ◽  
Trial Registry ◽  
Clinical Trial Registry ◽  
Clinical Trial Registration ◽  
Expression Levels ◽  
Inflammatory Bowel ◽  
Group 2

Abstract Objectives Inflammatory bowel disease (IBD) has multiple impacts on soft and hard tissues in the oral cavity. The aim of this study was to analyze the expression of cytokines in biofilm samples from patients suffering from IBD and compare them to healthy patients. It was hypothesized that different cytokine expression levels and clinical associations might be drawn. Material and methods A total of 56 biofilm samples from three different patient cohorts (group 0 = healthy, HC n = 30; group 1 = Crohn’s disease, CD, n = 19; group 2 = ulcerative colitis, UC, n = 7) were examined for the expression levels of the cytokine interleukins IL-2, -6, and -10; matrix metalloproteinases 7 and 9; and surface antigens CD90/CD11a by quantitative real-time PCR and according to clinical parameters (plaque index, BOP, PD, DMFT, CAL). Relative gene expression was determined using the ∆∆CT method. Results The mean BOP values (p = 0.001) and PD (p = 0.000) were significantly higher in the CD group compared to controls. Expression of IL-10 was significantly higher in the CD (p = 0.004) and UC groups (p = 0.022). Expression of MMP-7 was significantly higher in the CD group (p = 0.032). IBD patients treated with TNF inhibitors (p = 0.007) or other immunosuppressants (p = 0.014) showed significant overexpression of IL-10 compared to controls. Conclusion Different expression levels of IL-10 and MMP-7 were detected in plaque samples from IBD patients. As only BOP was significantly increased, we conclude that no clinical impairment of periodontal tissue occurred in IBD patients. Clinical relevance With the worldwide increasing incidence of IBD, it is important to obtain insights into the effects of the disease on the oral cavity. The study was registered (01.09.2020) at the German clinical trial registry (DRKS00022956). Clinical trial registration The study is registered at the German clinical trial registry (DRKS00022956).

Altered Fecal Bile Acid Pattern in Patients with Inflammatory Bowel Disease

Digestion ◽  
1986 ◽  
Vol 35 (4) ◽  
pp. 189-198 ◽  
Author(s):  
W. Kruis ◽  
H.-D. Kalek ◽  
F. Stellaard ◽  
G. Paumgartner
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Bowel Disease ◽  
Fecal Bile Acid ◽  
Inflammatory Bowel

scholarly journals Serum bile acid profiling reflects enterohepatic detoxification state and intestinal barrier function in inflammatory bowel disease

2009 ◽  
Vol 15 (25) ◽  
pp. 3134 ◽  
Author(s):  
Carsten Gnewuch ◽  
Gerhard Liebisch ◽  
Thomas Langmann ◽  
Benjamin Dieplinger ◽  
Thomas Mueller ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Bowel Disease ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Serum Bile Acid ◽  
Inflammatory Bowel

scholarly journals A Pilot Integrative Analysis of Colonic Gene Expression, Gut Microbiota, and Immune Infiltration in Primary Sclerosing Cholangitis-Inflammatory Bowel Disease: Association of Disease With Bile Acid Pathways

2020 ◽  
Vol 14 (7) ◽  
pp. 935-947 ◽  
Author(s):  
Mohammed Nabil Quraishi ◽  
Animesh Acharjee ◽  
Andrew D Beggs ◽  
Richard Horniblow ◽  
Chris Tselepis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Gut Microbiota ◽  
Primary Sclerosing Cholangitis ◽  
Bowel Disease ◽  
Sclerosing Cholangitis ◽  
16S Rrna Analysis ◽  
Immune Infiltration ◽  
Inflammatory Bowel

Abstract Background Although a majority of patients with PSC have colitis [PSC-IBD; primary sclerosing cholangitis-inflammatory bowel disease], this is phenotypically different from ulcerative colitis [UC]. We sought to define further the pathophysiological differences between PSC-IBD and UC, by applying a comparative and integrative approach to colonic gene expression, gut microbiota and immune infiltration data. Methods Colonic biopsies were collected from patients with PSC-IBD [n = 10], UC [n = 10], and healthy controls [HC; n = 10]. Shotgun RNA-sequencing for differentially expressed colonic mucosal genes [DEGs], 16S rRNA analysis for microbial profiling, and immunophenotyping were performed followed by multi-omic integration. Results The colonic transcriptome differed significantly between groups [p = 0.01]. Colonic transcriptomes from HC were different from both UC [1343 DEGs] and PSC-IBD [4312 DEGs]. Of these genes, only 939 had shared differential gene expression in both UC and PSC-IBD compared with HC. Imputed pathways were predominantly associated with upregulation of immune response and microbial defense in both disease cohorts compared with HC. There were 1692 DEGs between PSC-IBD and UC. Bile acid signalling pathways were upregulated in PSC-IBD compared with UC [p = 0.02]. Microbiota profiles were different between the three groups [p = 0.01]; with inferred function in PSC-IBD also being consistent with dysregulation of bile acid metabolism. Th17 cells and IL17-producing CD4 cells were increased in both PSC-IBD and UC when compared with HC [p < 0.05]. Multi-omic integration revealed networks involved in bile acid homeostasis and cancer regulation in PSC-IBD. Conclusions Colonic transcriptomic and microbiota analysis in PSC-IBD point toward dysregulation of colonic bile acid homeostasis compared with UC. This highlights important mechanisms and suggests the possibility of novel approaches in treating PSC-IBD.

Sa1785 - The Association of Serum 7A Hydroxy 4 Cholesten 3 One (7C4) with Bile Acid Diarrhea in Patients with Inflammatory Bowel Disease

2018 ◽  
Vol 154 (6) ◽  
pp. S-393
Author(s):  
Robert Battat ◽  
Marjolijn Duijvestein ◽  
Niels Vande Casteele ◽  
Siddharth Singh ◽  
Mark Renshaw ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bile Acid ◽  
Bowel Disease ◽  
Inflammatory Bowel

scholarly journals Silencing ferritin alleviates atherosclerosis in mice via regulating the expression levels of matrix metalloproteinases and interleukins

2021 ◽  
Author(s):  
Mei Zheng ◽  
Lizhuo Li ◽  
Yuqian Liu ◽  
Yun Liang ◽  
Xiaoyong Qi
Keyword(s):  
Matrix Metalloproteinases ◽  
Western Blot ◽  
Knockout Mice ◽  
Blot Analysis ◽  
High Fat Diet ◽  
Western Blot Analysis ◽  
High Fat ◽  
Expression Levels ◽  
Atherosclerotic Lesions ◽  
Apoe Knockout Mice

This study was conducted to investigate the roles of ferritin in atherosclerosis. The mouse model of atherosclerosis was established by feeding ApoE knockout mice with a high-fat diet. The mice were then treated with ferritin-overexpressing and -silencing constructs, and assessed for interleukins (ILs) and matrix metalloproteinases (MMPs) levels using ELISA and Western blot analysis. After being fed with a high-fat diet, the ApoE knockout mice developed pro-atherogenic lipid profiles with elevated total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C). They also showed increased atherosclerotic lesions including narrowed lumen diameter, reduced lumen area, and increased plaque size. Following injection of the overexpression and silencing constructs, mRNA levels of ferritin were increased and decreased, respectively, and at the same time the atherosclerotic lesions were aggravated and alleviated, respectively. Further analysis indicated that silencing of ferritin gene reduced IL-1β and IL-10 levels while overexpressing ferritin increased them. On other hand, the TNF-α levels showed an opposite trend. MMP8, MMP12 and MMP13 levels were increased or decreased significantly after the mice were injected with ferritin over-expression or silencing vectors, respectively. Western blot analysis showed that compared to the control, overexpressing ferritin resulted in increased expression of p-JNK while silencing ferritin decreased the expression. Meanwhile, the levels of pc-Jun remained unchanged. Our work demonstrates that ferritin can regulate the progress of atherosclerosis via regulating the expression levels of MMPs and interleukins. Silencing ferritin inhibits the development of atherosclerosis and is, therefore, worth being further investigated as a potential therapeutic approach for this disease.

scholarly journals PROTECTIVE EFFECT OF PHYLLANTHUS EMBLICA EXTRACT PREVENT CONTRAST-INDUCED ACUTE KIDNEY INJURY IN RATS

2019 ◽  
pp. 197-201
Author(s):  
SUPRANEE KONGKHAM ◽  
ADIS TASANARONG ◽  
ARUNPORN ITHARAT
Keyword(s):  
Acute Kidney Injury ◽  
Western Blot ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Kidney Injury ◽  
Saline Control ◽  
Phyllanthus Emblica ◽  
Rt Pcr ◽  
Expression Levels ◽  
Apoptotic Effect

Objective: The objective of the study was to investigate the anti-apoptosis effect of the extract from Phyllanthus emblica (PE) for the prevention of contrast-induced acute kidney injury (CI-AKI). Methods: Male Sprague Dawley rats were given saline (control) or PE extracts (500 mg/kg/day) for 5 days before the induction of CI-AKI. Renal tissues were collected for an evaluation of gene expression and immunohistochemistry (IHC). To indicate anti-apoptotic effect, the expression levels of Bax, Bcl-2, and caspase in kidney were also determined, using real-time polymerase chain reaction (RT-PCR) and Western blot analysis. Results: In the CI-AKI group, RT-PCR and Western blot analysis revealed that the expression levels of Bax and cleaved-caspase-3 were upregulated in the CI-AKI group, whereas the expression of Bcl-2 was downregulated. However, the pre-treatment with PE increased Bcl-2 expression. Moreover, decreased cleaved-caspases-3 activity was also detected using IHC. Conclusion: These findings suggested that pretreatment with PE extract provided the anti-apoptotic effect against CI-AKI in the rat model.

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