Evaluation of biomarkers for ulcerative colitis comparing two sampling methods: fecal markers reflect colorectal inflammation both macroscopically and on a cellular level

Peterson, Christer; Lampinen, Maria; Hansson, Tomas; Lidén, Maria; Hällgren, Roger; Carlson, Marie

doi:10.1080/00365513.2016.1185145

Cited by 19 publications

(21 citation statements)

References 39 publications

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“…Rats with DSS-induced colitis showed symptoms similar to those associated with UC patients, including diarrhea, body weight loss, bloody stool, and mucosal ulceration, and this model is used extensively for basic research and drug Berberine Upregulates P-Glycoprotein in Colitis discovery. In this study, using the DSS-induced colitis model, we observed neutrophil infiltration in colon tissues, as evidenced by increased MPO activity in the colonic mucosa, as well as splenomegaly, which is commonly reported in human UC (Ashrafi et al, 2014;Peterson et al, 2016) (Fig. 1).…”

Section: Discussionsupporting

confidence: 64%

Berberine Upregulates P-Glycoprotein in Human Caco-2 Cells and in an Experimental Model of Colitis in the Rat via Activation of Nrf2-Dependent Mechanisms

Jing

Safarpour

Zhang

et al. 2018

J Pharmacol Exp Ther

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Downregulation of P-glycoprotein (P-gp) is implicated in the pathophysiology of inflammatory bowel disease (IBD). Berberine, a principal isoquinoline alkaloid extracted from species, has been reported to exhibit therapeutic potential in IBD. In this study, we used a dextran sulfate sodium (DSS)-induced colitis rat model to evaluate the effect of berberine on P-gp and explore its mechanism of action. Berberine treatment improved DSS-induced colitis symptoms, attenuated inflammatory markers (myeloperoxidase, tumor necrosis factor-, and interleukin-1 and -6), and enhanced P-gp expression in a dose-dependent manner. Although colonic expression of the P-gp-related nuclear receptor pregnane X receptor and transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) were downregulated in the colitis model, gene and protein expression analysis revealed that berberine treatment reversed only the downregulation of Nrf2. In vitro studies using Caco-2 cells showed that the multidrug resistance 1 () gene and P-gp protein were upregulated by berberine in a dose- and time-dependent manner. Significant upregulation of the gene by berberine was abrogated by Nrf2 silencing, indicating that the Nrf2-mediated pathway was responsible for this activation. Luciferase assays showed a dose-dependent increase in Nrf2 reporter gene activity after berberine treatment in Caco-2 cells, with a significant 2-fold elevation at 2.5M berberine, suggesting that berberine is a strong Nrf2 activator. These results indicate the possible involvement of Nrf2-mediated upregulation of P-gp in the therapeutic effect of berberine on colitis and highlight the potential of P-gp and/or Nrf2 as new therapeutic targets for IBD.

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Section: Discussionsupporting

confidence: 64%

Berberine Upregulates P-Glycoprotein in Human Caco-2 Cells and in an Experimental Model of Colitis in the Rat via Activation of Nrf2-Dependent Mechanisms

Jing

Safarpour

Zhang

et al. 2018

J Pharmacol Exp Ther

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“…The fact that fecal eosinophil granular proteins are elevated in patients with IBD has been shown by several recent studies [35][36][37][38][39][40][41]. However, these studies were performed in smaller cohorts than in our study.…”

Section: Discussionmentioning

confidence: 56%

“…Clinical follow-up data was available for 202/212 visits (95.3%) of patients with IBD. The median (IQR) follow-up time was 48 (38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50)(51)(52)(53)(54) months. The total event rate was 94/202 (46.5%).…”

Section: Fecp Is a Prognostic Biomarker In Young Patients With Ibdmentioning

confidence: 99%

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Fecal Eosinophil Cationic Protein Is a Diagnostic and Predictive Biomarker in Young Adults with Inflammatory Bowel Disease

Abedin

Seemann

Kleinfeld

et al. 2019

JCM

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Background and Aims: Fecal biomarkers are important non-invasive markers monitoring disease activity in inflammatory bowel disease (IBD). We compared the significance of fecal eosinophil cationic protein (fECP) and fecal calprotectin (fCal). Methods: fECP and fCal were measured in patients with Crohn’s disease (CD, n = 97), ulcerative colitis (UC, n = 53), Clostridioides difficile infection (CDI, n = 9), primary food allergy (PFA, n = 11), pollen-associated food allergy (n = 25) and non-inflammatory controls (n = 78). Results were correlated with clinical and endoscopic IBD activity scores. Results: fECP was significantly elevated in CD, UC, CDI and PFA compared to controls. fCal was significantly increased in CD, UC and CDI. fECP had lower diagnostic accuracy than fCal (area under the curve (AUC) = 0.88) in differentiating between endoscopically active and inactive patients with IBD (AUC = 0.77, ROC analysis). In contrast to fCal, fECP correlated negatively with age and levels were also elevated in clinically and endoscopically inactive patients with IBD <45 years (endoscopically inactive IBD vs controls; AUC for fECP = 0.86; AUC for fCal = 0.62). However, in those patients with low inflammatory activity (fCal <250 mg/kg), high fECP indicated the need for treatment modification or surgery (fECP <200 µg/kg = 22%; 200–600 µg/kg = 44%; >600 µg/kg = 82%) at month 48 of follow-up. Conclusions: fECP is a diagnostic and prognostic marker in young patients with IBD in remission.

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“…Further evidence of FAC involvement in inflammasome activation was provided by Thinwa et al [43] who demonstrated that the initial signal for intestinal cell inflammasome activation in pathogen recognition is via integrins. It is interesting to note that NLRP3 was identified as a candidate gene for susceptibility of Crohn’s disease [44], whereas IL-1 has been put forward as a faecal marker of inflammation in UC [45].…”

Section: Introductionmentioning

confidence: 99%

Omics Approaches to Identify Potential Biomarkers of Inflammatory Diseases in the Focal Adhesion Complex

Brooks

Watson

Korcsmáros

2017

Genomics, Proteomics &Amp; Bioinformatics

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Inflammatory diseases such as inflammatory bowel disease (IBD) require recurrent invasive tests, including blood tests, radiology, and endoscopic evaluation both to diagnose and assess disease activity, and to determine optimal therapeutic strategies. Simple ‘bedside’ biomarkers could be used in all phases of patient management to avoid unnecessary investigation and guide further management. The focal adhesion complex (FAC) has been implicated in the pathogenesis of multiple inflammatory diseases, including IBD, rheumatoid arthritis, and multiple sclerosis. Utilizing omics technologies has proven to be an efficient approach to identify biomarkers from within the FAC in the field of cancer medicine. Predictive biomarkers are paving the way for the success of precision medicine for cancer patients, but inflammatory diseases have lagged behind in this respect. This review explores the current status of biomarker prediction for inflammatory diseases from within the FAC using omics technologies and highlights the benefits of future potential biomarker identification approaches.

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Evaluation of biomarkers for ulcerative colitis comparing two sampling methods: fecal markers reflect colorectal inflammation both macroscopically and on a cellular level

Cited by 19 publications

References 39 publications

Berberine Upregulates P-Glycoprotein in Human Caco-2 Cells and in an Experimental Model of Colitis in the Rat via Activation of Nrf2-Dependent Mechanisms

Berberine Upregulates P-Glycoprotein in Human Caco-2 Cells and in an Experimental Model of Colitis in the Rat via Activation of Nrf2-Dependent Mechanisms

Fecal Eosinophil Cationic Protein Is a Diagnostic and Predictive Biomarker in Young Adults with Inflammatory Bowel Disease

Omics Approaches to Identify Potential Biomarkers of Inflammatory Diseases in the Focal Adhesion Complex

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