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  1. Article: Resveratrol Downregulates miR‐31 to Promote T Regulatory Cells during Prevention of TNBS‐Induced Colitis

    Alrafas, Haider Rasheed / Busbee, Philip B / Nagarkatti, Mitzi / Nagarkatti, Prakash S

    Molecular nutrition & food research. 2020 Jan., v. 64, no. 1

    2020  

    Abstract: SCOPE: Colitis, an inflammatory bowel disease, is associated with aberrant regulation of the colonic mucosal immune system. Resveratrol, a natural plant product, has been found to exert anti‐inflammatory properties and attenuate the development of murine ...

    Abstract SCOPE: Colitis, an inflammatory bowel disease, is associated with aberrant regulation of the colonic mucosal immune system. Resveratrol, a natural plant product, has been found to exert anti‐inflammatory properties and attenuate the development of murine colitis. In the current study, the role of microRNA (miR) in the ability of resveratrol to suppress colonic inflammation is examined. METHODS AND RESULTS: BALB/C mice with 2,4,6‐Trinitrobenzenesulfonic acid solution (TNBS)‐induced colitis, when treated with resveratrol, show improved clinical outcomes and reduce induction of inflammatory T cells (Th17 and Th1) while increasing CD4+Foxp3+ regulatory T cells (Tregs) and IL‐10‐producing CD4+ T cells. miR microarray analysis and polymerase chain reaction (PCR) validation from CD4+ T cells show treatment with resveratrol decreases the expression of several miRs (miR‐31, Let7a, miR‐132) that targets cytokines and transcription factors involved in anti‐inflammatory T cell responses (Foxp3 and TGF‐β). Transfection studies with miR‐31 confirm that this miR directly regulates the expression of Foxp3. Lastly, analysis of public data from human patients with ulcerative colitis reveals that miR‐31 expression is significantly increased when compared to controls. CONCLUSION: Together, the current study demonstrates that resveratrol‐mediated attenuation of colitis may be regulated by miR‐31 through induction of Tregs and miR‐31 may serve as a therapeutic target for human colitis.
    Keywords CD4-positive T-lymphocytes ; anti-inflammatory activity ; cytokines ; human diseases ; inflammation ; mice ; microRNA ; microarray technology ; mucosal immunity ; patients ; plant products ; polymerase chain reaction ; resveratrol ; sulfonic acids ; therapeutics ; transcription factors ; transfection ; transforming growth factor beta ; ulcerative colitis
    Language English
    Dates of publication 2020-01
    Publishing place John Wiley & Sons, Ltd
    Document type Article
    Note JOURNAL ARTICLE
    ZDB-ID 2160372-8
    ISSN 1613-4133 ; 1613-4125
    ISSN (online) 1613-4133
    ISSN 1613-4125
    DOI 10.1002/mnfr.201900633
    Database NAL-Catalogue (AGRICOLA)

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  2. Article ; Online: Resveratrol Downregulates miR-31 to Promote T Regulatory Cells during Prevention of TNBS-Induced Colitis.

    Alrafas, Haider Rasheed / Busbee, Philip B / Nagarkatti, Mitzi / Nagarkatti, Prakash S

    Molecular nutrition & food research

    2019  Volume 64, Issue 1, Page(s) e1900633

    Abstract: Scope: Colitis, an inflammatory bowel disease, is associated with aberrant regulation of the colonic mucosal immune system. Resveratrol, a natural plant product, has been found to exert anti-inflammatory properties and attenuate the development of ... ...

    Abstract Scope: Colitis, an inflammatory bowel disease, is associated with aberrant regulation of the colonic mucosal immune system. Resveratrol, a natural plant product, has been found to exert anti-inflammatory properties and attenuate the development of murine colitis. In the current study, the role of microRNA (miR) in the ability of resveratrol to suppress colonic inflammation is examined.
    Methods and results: BALB/C mice with 2,4,6-Trinitrobenzenesulfonic acid solution (TNBS)-induced colitis, when treated with resveratrol, show improved clinical outcomes and reduce induction of inflammatory T cells (Th17 and Th1) while increasing CD4+Foxp3+ regulatory T cells (Tregs) and IL-10-producing CD4+ T cells. miR microarray analysis and polymerase chain reaction (PCR) validation from CD4+ T cells show treatment with resveratrol decreases the expression of several miRs (miR-31, Let7a, miR-132) that targets cytokines and transcription factors involved in anti-inflammatory T cell responses (Foxp3 and TGF-β). Transfection studies with miR-31 confirm that this miR directly regulates the expression of Foxp3. Lastly, analysis of public data from human patients with ulcerative colitis reveals that miR-31 expression is significantly increased when compared to controls.
    Conclusion: Together, the current study demonstrates that resveratrol-mediated attenuation of colitis may be regulated by miR-31 through induction of Tregs and miR-31 may serve as a therapeutic target for human colitis.
    MeSH term(s) Animals ; Case-Control Studies ; Colitis/chemically induced ; Colitis/drug therapy ; Colitis/genetics ; Colitis/prevention & control ; Colitis, Ulcerative/genetics ; Down-Regulation/drug effects ; Female ; Forkhead Transcription Factors/genetics ; Forkhead Transcription Factors/metabolism ; Gene Expression Regulation/drug effects ; Humans ; Mice, Inbred C57BL ; MicroRNAs/genetics ; Resveratrol/pharmacology ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/physiology ; Th17 Cells/drug effects ; Trinitrobenzenesulfonic Acid/toxicity
    Chemical Substances Forkhead Transcription Factors ; Foxp3 protein, mouse ; MIRN31 microRNA, human ; MicroRNAs ; Mirn31 microRNA, mouse ; Trinitrobenzenesulfonic Acid (8T3HQG2ZC4) ; Resveratrol (Q369O8926L)
    Language English
    Publishing date 2019-12-11
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2160372-8
    ISSN 1613-4133 ; 1613-4125
    ISSN (online) 1613-4133
    ISSN 1613-4125
    DOI 10.1002/mnfr.201900633
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Resveratrol modulates the gut microbiota to prevent murine colitis development through induction of Tregs and suppression of Th17 cells.

    Alrafas, Haider Rasheed / Busbee, Philip B / Nagarkatti, Mitzi / Nagarkatti, Prakash S

    Journal of leukocyte biology

    2019  Volume 106, Issue 2, Page(s) 467–480

    Abstract: Inflammatory diseases of the gastrointestinal tract are often associated with microbial dysbiosis. Thus, dietary interactions with intestinal microbiota, to maintain homeostasis, play a crucial role in regulation of clinical disorders such as colitis. In ...

    Abstract Inflammatory diseases of the gastrointestinal tract are often associated with microbial dysbiosis. Thus, dietary interactions with intestinal microbiota, to maintain homeostasis, play a crucial role in regulation of clinical disorders such as colitis. In the current study, we investigated if resveratrol, a polyphenol found in a variety of foods and beverages, would reverse microbial dysbiosis induced during colitis. Administration of resveratrol attenuated colonic inflammation and clinical symptoms in the murine model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Resveratrol treatment in mice with colitis led to an increase in CD4
    MeSH term(s) Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology ; Biomarkers ; Colitis/etiology ; Colitis/metabolism ; Colitis/pathology ; Colitis/prevention & control ; Colonoscopy ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Female ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Microbiome/immunology ; Humans ; Immunomodulation/drug effects ; Metagenomics/methods ; Mice ; Resveratrol/pharmacology ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Th17 Cells/drug effects ; Th17 Cells/immunology ; Th17 Cells/metabolism
    Chemical Substances Anti-Inflammatory Agents, Non-Steroidal ; Biomarkers ; Resveratrol (Q369O8926L)
    Language English
    Publishing date 2019-03-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 605722-6
    ISSN 1938-3673 ; 0741-5400
    ISSN (online) 1938-3673
    ISSN 0741-5400
    DOI 10.1002/JLB.3A1218-476RR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 603: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article: Alterations in the Gut Microbiome and Suppression of Histone Deacetylases by Resveratrol Are Associated with Attenuation of Colonic Inflammation and Protection Against Colorectal Cancer.

    Alrafas, Haider Rasheed / Busbee, Philip Brandon / Chitrala, Kumaraswamy Naidu / Nagarkatti, Mitzi / Nagarkatti, Prakash

    Journal of clinical medicine

    2020  Volume 9, Issue 6

    Abstract: Inflammatory bowel disease (IBD) is known to significantly increase the risk for development of colorectal cancer (CRC), suggesting inflammation and cancer development are closely intertwined. Thus, agents that suppress inflammation may prevent the onset ...

    Abstract Inflammatory bowel disease (IBD) is known to significantly increase the risk for development of colorectal cancer (CRC), suggesting inflammation and cancer development are closely intertwined. Thus, agents that suppress inflammation may prevent the onset of cancer. In the current study, we used resveratrol, an anti-inflammatory stilbenoid, to study the role of microbiota in preventing inflammation-driven CRC. Resveratrol treatment in the azoxymethane (AOM) and dextran sodium sulphate (DSS) CRC murine model caused an increase in anti-inflammatory CD4 + FOXP3 + (Tregs) and CD4 + IL10 + cells, a decrease in proinflammatory Th1 and Th17 cells, and attenuated CRC development. Gut microbial profile studies demonstrated that resveratrol altered the gut microbiome and short chain fatty acid (SCFA), with modest increases in n-butyric acid and a potential butyrate precursor isobutyric acid. Fecal transfer from resveratrol-treated CRC mice and butyrate supplementation resulted in attenuation of disease and suppression of the inflammatory T cell response. Data also revealed both resveratrol and sodium butyrate (BUT) were capable of inhibiting histone deacetylases (HDACs), correlating with Treg induction. Analysis of The Cancer Genome Atlas (TCGA) datasets revealed increased expression of Treg-specific transcription factor FoxP3 or anti-inflammatory IL-10 resulted in an increase in 5-year survival of patients with CRC. These data suggest that alterations in the gut microbiome lead to an anti-inflammatory T cell response, leading to attenuation of inflammation-driven CRC.
    Language English
    Publishing date 2020-06-09
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662592-1
    ISSN 2077-0383
    ISSN 2077-0383
    DOI 10.3390/jcm9061796
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Activation of Cannabinoid Receptor 2 Prevents Colitis-Associated Colon Cancer through Myeloid Cell De-activation Upstream of IL-22 Production.

    Becker, William / Alrafas, Haider Rasheed / Wilson, Kiesha / Miranda, Kathryn / Culpepper, Courtney / Chatzistamou, Ioulia / Cai, Guoshuai / Nagarkatti, Mitzi / Nagarkatti, Prakash S

    iScience

    2020  Volume 23, Issue 9, Page(s) 101504

    Abstract: Intestinal disequilibrium leads to inflammatory bowel disease (IBD), and chronic inflammation predisposes to oncogenesis. Antigen-presenting dendritic cells (DCs) and macrophages can tip the equilibrium toward tolerance or pathology. Here we show that ... ...

    Abstract Intestinal disequilibrium leads to inflammatory bowel disease (IBD), and chronic inflammation predisposes to oncogenesis. Antigen-presenting dendritic cells (DCs) and macrophages can tip the equilibrium toward tolerance or pathology. Here we show that delta-9-tetrahydrocannabinol (THC) attenuates colitis-associated colon cancer and colitis induced by anti-CD40. Working through cannabinoid receptor 2 (CB2), THC increases CD103 expression on DCs and macrophages and upregulates TGF-β1 to increase T regulatory cells (Tregs). THC-induced Tregs are necessary to remedy systemic IFNγ and TNFα caused by anti-CD40, but CB2-mediated suppression of APCs by THC quenches pathogenic release of IL-22 and IL-17A in the colon. By examining tissues from multiple sites, we confirmed that THC affects DCs, especially in mucosal barrier sites in the colon and lungs, to reduce DC CD86. Using models of colitis and systemic inflammation we show that THC, through CB2, is a potent suppressor of aberrant immune responses by provoking coordination between APCs and Tregs.
    Language English
    Publishing date 2020-08-27
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2020.101504
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Cannabinoid Receptor Activation on Haematopoietic Cells and Enterocytes Protects against Colitis.

    Becker, William / Alrafas, Haider Rasheed / Busbee, Philip B / Walla, Michael D / Wilson, Kiesha / Miranda, Kathryn / Cai, Guoshuai / Putluri, Vasanta / Putluri, Nagireddy / Nagarkatti, Mitzi / Nagarkatti, Prakash S

    Journal of Crohn's & colitis

    2020  Volume 15, Issue 6, Page(s) 1032–1048

    Abstract: Background and aims: Cannabinoid receptor [CB] activation can attenuate inflammatory bowel disease [IBD] in experimental models and human cohorts. However, the roles of the microbiome, metabolome, and the respective contributions of haematopoietic and ... ...

    Abstract Background and aims: Cannabinoid receptor [CB] activation can attenuate inflammatory bowel disease [IBD] in experimental models and human cohorts. However, the roles of the microbiome, metabolome, and the respective contributions of haematopoietic and non-haematopoietic cells in the anti-colitic effects of cannabinoids have yet to be determined.
    Methods: Female C57BL/6 mice were treated with either cannabidiol [CBD], Δ 9-tetrahydrocannabinol [THC], a combination of CBD and THC, or vehicle, in several models of chemically induced colitis. Clinical parameters of colitis were assessed by colonoscopy, histology, flow cytometry, and detection of serum biomarkers; single-cell RNA sequencing and qRT-PCR were used to evaluate the effects of cannabinoids on enterocytes. Immune cell transfer from CB2 knockout mice was used to evaluate the contribution of haematopoietic and non-haematopoietic cells to colitis protection.
    Results: We found that THC prevented colitis and that CBD, at the dose tested, provided little benefit to the amelioration of colitis, nor when added synergistically with THC. THC increased colonic barrier integrity by stimulating mucus and tight junction and antimicrobial peptide production, and these effects were specific to the large intestine. THC increased colonic Gram-negative bacteria, but the anti-colitic effects of THC were independent of the microbiome. THC acted both on immune cells via CB2 and on enterocytes, to attenuate colitis.
    Conclusions: Our findings demonstrate how cannabinoid receptor activation on both immune cells and colonocytes is critical to prevent colonic inflammation. These studies also suggest how cannabinoid receptor activation can be used as a preventive and therapeutic modality against colitis.
    MeSH term(s) Animals ; Cannabidiol/pharmacology ; Cannabinoid Receptor Agonists/pharmacology ; Colitis/chemically induced ; Colitis/metabolism ; Colitis/pathology ; Colitis/therapy ; Colonoscopy/methods ; Dronabinol/pharmacology ; Drug Monitoring ; Enterocytes/drug effects ; Enterocytes/metabolism ; Enterocytes/pathology ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Microbiome/immunology ; Immunity, Cellular/drug effects ; Immunity, Cellular/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Protective Agents/pharmacology ; Receptor, Cannabinoid, CB2/genetics ; Receptor, Cannabinoid, CB2/metabolism
    Chemical Substances Cannabinoid Receptor Agonists ; Protective Agents ; Receptor, Cannabinoid, CB2 ; Cannabidiol (19GBJ60SN5) ; Dronabinol (7J8897W37S)
    Language English
    Publishing date 2020-12-17
    Publishing country England
    Document type Journal Article
    ZDB-ID 2390120-2
    ISSN 1876-4479 ; 1873-9946
    ISSN (online) 1876-4479
    ISSN 1873-9946
    DOI 10.1093/ecco-jcc/jjaa253
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6634: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Indole-3-carbinol prevents colitis and associated microbial dysbiosis in an IL-22-dependent manner.

    Busbee, Philip B / Menzel, Lorenzo / Alrafas, Haider Rasheed / Dopkins, Nicholas / Becker, William / Miranda, Kathryn / Tang, Chaunbing / Chatterjee, Saurabh / Singh, Udai / Nagarkatti, Mitzi / Nagarkatti, Prakash S

    JCI insight

    2020  Volume 5, Issue 1

    Abstract: Colitis, an inflammatory bowel disease, is caused by a variety of factors, but luminal microbiota are thought to play crucial roles in disease development and progression. Indole is produced by gut microbiota and is believed to protect the colon from ... ...

    Abstract Colitis, an inflammatory bowel disease, is caused by a variety of factors, but luminal microbiota are thought to play crucial roles in disease development and progression. Indole is produced by gut microbiota and is believed to protect the colon from inflammatory damage. In the current study, we investigated whether indole-3-carbinol (I3C), a naturally occurring plant product found in numerous cruciferous vegetables, can prevent colitis-associated microbial dysbiosis and attempted to identify the mechanisms. Treatment with I3C led to repressed colonic inflammation and prevention of microbial dysbiosis caused by colitis, increasing a subset of gram-positive bacteria known to produce butyrate. I3C was shown to increase production of butyrate, and when mice with colitis were treated with butyrate, there was reduced colonic inflammation accompanied by suppression of Th17 and induction of Tregs, protection of the mucus layer, and upregulation in Pparg expression. Additionally, IL-22 was increased only after I3C but not butyrate administration, and neutralization of IL-22 prevented the beneficial effects of I3C against colitis, as well as blocked I3C-mediated dysbiosis and butyrate induction. This study suggests that I3C attenuates colitis primarily through induction of IL-22, which leads to modulation of gut microbiota that promote antiinflammatory butyrate.
    MeSH term(s) Animals ; Butyric Acid/metabolism ; Butyric Acid/pharmacology ; Colitis/metabolism ; Colitis/pathology ; Colitis/prevention & control ; Colon/drug effects ; Colon/microbiology ; Colon/pathology ; Disease Models, Animal ; Dysbiosis/microbiology ; Dysbiosis/prevention & control ; Female ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Microbiome/genetics ; Indoles/pharmacology ; Indoles/therapeutic use ; Inflammation/prevention & control ; Interleukins/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; RNA, Ribosomal, 16S/genetics ; Th17 Cells ; Interleukin-22
    Chemical Substances Indoles ; Interleukins ; RNA, Ribosomal, 16S ; Butyric Acid (107-92-6) ; indole-3-carbinol (C11E72455F)
    Language English
    Publishing date 2020-01-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.127551
    Database MEDical Literature Analysis and Retrieval System OnLINE

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