Exosome-Induced Regulation in Inflammatory Bowel Disease

Zhang, Huiting; Wang, Liang; Li, Changyi; Yu, Yue; Yi, Yanlin; Wang, Jingyu; Chen, Dapeng

doi:10.3389/fimmu.2019.01464

Cited by 112 publications

(85 citation statements)

References 81 publications

(105 reference statements)

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“…Research shows that following treatment with Fructus Meliae Toosendan (a known hepatotoxic TCM), 8 miRNAs and 1,723 mRNAs were significantly differentially expressed (Zheng et al, 2015). Other studies found that miRNA374a, tumor necrosis factor receptor, and exosomes were related to the mechanism of inflammatory bowel disease, and recent evidence supports that hepatocyte-derived exosomes play a key role in the pathogenesis of DILI (Zhou et al, 2017;Thacker et al, 2018;Xiong et al, 2018;Zhang et al, 2019). These studies provide new insights into these potential biomarkers for TCM-induced liver injury.…”

Section: Future Prospects and Studiesmentioning

confidence: 81%

Molecular Biomarkers in Drug-Induced Liver Injury: Challenges and Future Perspectives

Jiang

et al. 2020

Front. Pharmacol.

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Drug-induced liver injury (DILI) is one among the common adverse drug reactions and the leading causes of drug development attritions, black box warnings, and post-marketing withdrawals. Despite having relatively low clinical incidence, its potentially severe adverse events should be considered in the individual patients due to the high risk of acute liver failure. Although traditional liver parameters have been applied to the diagnosis of DILI, the lack of specific and sensitive biomarkers poses a major limitation, and thus accurate prediction of the subsequent clinical course remains a significant challenge. These drawbacks prompt the investigation and discovery of more effective biomarkers, which could lead to early detection of DILI, and improve its diagnosis and prognosis. Novel promising biomarkers include glutamate dehydrogenase, keratin 18, sorbitol dehydrogenase, glutathione S-transferase, bile acids, cytochrome P450, osteopontin, high mobility group box-1 protein, fatty acid binding protein 1, cadherin 5, miR-122, genetic testing, and omics technologies, among others. Furthermore, several clinical scoring systems have gradually emerged for the diagnosis of DILI including the Roussel Uclaf Causality Assessment Method (RUCAM), Clinical Diagnostic Scale (CDS), and Digestive Disease Week Japan (DDW-J) systems. However, currently their predictive value is limited with certain inherent deficiencies. Thus, perhaps the greatest benefit would be achieved by simultaneously combining the scoring systems and those biomarkers. Herein, we summarized the recent research progress on molecular biomarkers for DILI to improved approaches for its diagnosis and clinical management.

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Section: Future Prospects and Studiesmentioning

confidence: 81%

Molecular Biomarkers in Drug-Induced Liver Injury: Challenges and Future Perspectives

Jiang

et al. 2020

Front. Pharmacol.

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“…Hence, efforts to investigate the biogenetic mechanisms and functional studies should be undertaken. These studies would provide helpful clues for the development of new therapeutics based on modulation of ApoExo release in human diseases and promote future use of these molecules as vehicles of drug delivery and gene therapy similar to exosomes [72][73][74][75] . Fig.…”

Section: Discussionmentioning

confidence: 99%

Apoptotic cell-derived exosomes: messages from dying cells

et al. 2020

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Apoptosis, a type of programmed cell death that plays a key role in both healthy and pathological conditions, releases extracellular vesicles such as apoptotic bodies and microvesicles, but exosome release due to apoptosis is not yet commonly accepted. Here, the reports demonstrating the presence of apoptotic exosomes and their roles in inflammation and immune responses are summarized, together with a general summary of apoptosis and extracellular vesicles. In conclusion, apoptosis is not just a 'silent' type of cell death but an active form of communication from dying cells to live cells through exosomes.

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“…[ 6 ] Besides, immune cell-related barrier loss, especially induced by exosomes, also influences the function of intestinal barrier. [ 7 ] The intestinal epithelial barrier is manipulated by epithelial cell secretory and transporting defenses (mucus, antimicrobial proteins, and immunoglobulin A), the apoptosis/proliferation of epithelial cells, and cell junctions like adherens junction and tight junction (TJ). [ 8 ]…”

Section: Introductionmentioning

confidence: 99%

Salvianolic acid B decreases interleukin-1β-induced colitis recurrence in mice

Feng

Fang

Zhao

et al. 2020

Chinese Medical Journal

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Background Degree of mucosal recovery is an important indicator for evaluating the therapeutic effects of drugs in treatment of inflammatory bowel disease (IBD). Increasing evidences has proved that tight junction (TJ) barrier dysfunction is one of the pathological mechanisms of IBD. The aim of this study was to observe whether enhancement of TJ can decrease colitis recurrence. Methods Eighty C57BL/6 mice were randomly divided into four groups including normal group, colitis group, sulfasalazine (SASP) treated group, and traditional Chinese drug salvianolic acid B (Sal B) treated group. Colitis was established in mice by free drinking water containing dextran sulfate sodium, after treatments by SASP and Sal B, recombinant human interleukin-1β (IL-1β) was injected intraperitoneally to induce colitis recurrence. Results Compared with sham control, cell apoptosis in colitis group was increased from 100.85 ± 3.46% to 162.89 ± 11.45% ( P = 0.0038), and TJ dysfunction marker myosin light chain kinase (MLCK) was also significantly increased from 99.70 ± 9.29% to 296.23 ± 30.78% ( P = 0.0025). The increased cell apoptosis was reversed by both SASP (125.99 ± 8.45% vs. 162.89 ± 11.45%, P = 0.0059) and Sal B (104.27 ± 6.09% vs. 162.89 ± 11.45%, P = 0.0044). High MLCK expression in colitis group was reversed by Sal B (182.44 ± 89.42% vs. 296.23 ± 30.78%, P = 0.0028) but not influenced by SASP (285.23 ± 41.04% vs. 296.23 ± 30.78%, P > 0.05). The recurrence rate induced by recombinant human IL-1β in Sal B-treated group was significantly lower than that in SASP-treated group. Conclusions These results suggested a link between intestinal mucosal barrier dysfunction, especially TJ barrier dysfunction, and colitis recurrence. The TJ barrier dysfunction in remission stage of colitis increased the colitis recurrence. This study might provide potential treatment strategies for IBD recurrence.

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Exosome-Induced Regulation in Inflammatory Bowel Disease

Cited by 112 publications

References 81 publications

Molecular Biomarkers in Drug-Induced Liver Injury: Challenges and Future Perspectives

Molecular Biomarkers in Drug-Induced Liver Injury: Challenges and Future Perspectives

Apoptotic cell-derived exosomes: messages from dying cells

Salvianolic acid B decreases interleukin-1β-induced colitis recurrence in mice

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