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Is Inflammatory bowel disease reversible

Zhen Zhang, Kyaw Min Aung, Bernt Eric Uhlin, Sun Nyunt Wai
Cytotoxic necrotizing factor 1 (CNF1), a protein toxin produced by extraintestinal pathogenic Escherichia coli, activates the Rho-family small GTPases in eukaryotic cell, thereby perturbing multiple cellular functions. Increasing epidemiological evidence suggests a link between CNF1 and human inflammatory bowel disease and colorectal cancer. At the cellular level, CNF1 has been hypothesized to reprogram cell fate towards survival due to the role in perturbing cell cycle and apoptosis. However, it remains undetermined how cells survive from CNF1 intoxication...
December 12, 2018: Scientific Reports
Xiaodong Zhu, Ye Zhu, Caijuan Li, Jianbo Yu, DanDan Ren, Shou Qiu, Ying Nie, Xin Yu, Xiaoyan Xu, Wei Zhu
Macrophages are highly plastic cells. Depending on stimulation, macrophages rapidly polarize to functionally distinct phenotypes that are involved in the pathogenesis of inflammatory bowel disease (IBD). 1,25‑Dihydroxyvitamin D (1,25(OH)2 D3 ) has immunomodulatory activity, and 1,25(OH)2 D3 deficiency is correlated with autoimmune diseases, especially IBD. This study aimed to explore whether 1,25(OH)2 D3 modulates macrophage polarization in inflammation. Peripheral blood mononuclear cells and colitis mice were treated with 1,25(OH)2 D3 ...
December 9, 2018: International Immunopharmacology
Daniel A Giles, Sonja Zahner, Petra Krause, Esmé Van Der Gracht, Thomas Riffelmacher, Venetia Morris, Alexei Tumanov, Mitchell Kronenberg
Over 1.5 million individuals in the United States are afflicted with inflammatory bowel disease (IBD). While the progression of IBD is multifactorial, chronic, unresolved inflammation certainly plays a key role. Additionally, while multiple immune mediators have been shown to affect pathogenesis, a comprehensive understanding of disease progression is lacking. Previous work has demonstrated that a member of the TNF superfamily, TNFSF14 (LIGHT), which is pro-inflammatory in several contexts, surprisingly plays an important role in protection from inflammation in mouse models of colitis, with LIGHT deficient mice having more severe disease pathogenesis...
2018: Frontiers in Immunology
Takafumi Kawamura, Masayoshi Yamamoto, Katsunori Suzuki, Yuhi Suzuki, Megumu Kamishima, Mayu Sakata, Kiyotaka Kurachi, Mitsutoshi Setoh, Hiroyuki Konno, Hiroya Takeuchi
Background: Colitis-associated cancer (CAC) is one of the prognostic factors in inflammatory bowel disease (IBD), and prevention of CAC is a critical concern for patients with IBD. Component cells of the microenvironment, especially myofibroblasts, are known to affect tumor development, but the role of intestinal myofibroblasts (IMFs) in CAC has not been clarified. Here, we explored the role of IMFs in CAC and sought to identify candidate genes as novel therapeutic targets for the prevention of CAC...
December 4, 2018: Inflammatory Bowel Diseases
Adebowale O Bamidele, Phyllis A Svingen, Mary R Sagstetter, Olga F Sarmento, Michelle Gonzalez, Manuel B Braga Neto, Subra Kugathasan, Gwen Lomberk, Raul A Urrutia, William A Faubion
Background & Aims: Forkhead box protein 3 (FOXP3)+ regulatory T cell (Treg) dysfunction is associated with autoimmune diseases; however, the mechanisms responsible for inflammatory bowel disease pathophysiology are poorly understood. Here, we tested the hypothesis that a physical interaction between transcription factor FOXP3 and the epigenetic enzyme enhancer of zeste homolog 2 (EZH2) is essential for gene co-repressive function. Methods: Human FOXP3 mutations clinically relevant to intestinal inflammation were generated by site-directed mutagenesis...
2019: Cellular and Molecular Gastroenterology and Hepatology
Sharmistha Banerjee, Sumit Ghosh, Krishnendu Sinha, Sayantani Chowdhury, Parames C Sil
Colitis is an inflammatory disease of the gastrointestinal tract. Inflammation, oxidative stress and cell death constitute the backbone of colitis. Most of the drugs prescribed for inflammatory bowel disease (IBD) have various side effects. In this scenario, we would like to determine the therapeutic role sulphur dioxide, a gaso-transmitter produced through the metabolism of cysteine in colitis. Colitis was induced through intrarectal administration of 2,4,6-trinitrobenzenesulfonic acid (TNBS) in male Wistar rats...
November 29, 2018: Toxicology
Jingru Zhang, Bo Lian, Yan Shang, Chun Li, Qingkai Meng
BACKGROUND/AIMS: miR-135a is reduced in several cancers and has been suggested to mediate immune and inflammatory responses. However, the effect of miR-135a on inflammatory bowel diseases was obscure. This study firstly attempted to investigate the hypothesis that miR-135a alleviates dextran sodium sulfate (DSS)-induced inflammation in colonic cells and potential mechanisms are also studied. METHODS: Caco-2 and HT-29 cells in this study were treated with DSS, miR-135a mimic, and S3I-201, and then CKK-8 assay was used to test cell viability...
2018: Cellular Physiology and Biochemistry
Xiaoming Hu, Jiali Deng, Tianming Yu, Shanghai Chen, Yadong Ge, Ziheng Zhou, Yajie Guo, Hao Ying, Qiwei Zhai, Yan Chen, Feixiang Yuan, Yuguo Niu, Weigang Shu, Huimin Chen, Caiyun Ma, Zhanju Liu, Feifan Guo
BACKGROUND & AIMS: Activating transcription factor 4 (ATF4) regulates genes involved in the inflammatory response, amino acid metabolism, autophagy, and endoplasmic reticulum stress. We investigated whether its activity is altered in patients with inflammatory bowel diseases (IBD) and mice with enterocolitis. METHODS: We obtained biopsy samples during endoscopy from inflamed and/or uninflamed regions of colon from 21 patients with active CD, 22 patients with active UC, and 38 individuals without IBD (controls), and of ileum from 19 patients with active CD and 8 individuals without IBD in China...
November 16, 2018: Gastroenterology
Huan Zhou, Hui-Jing Zhang, Lin Guan, Yi-Ning Zhang, Yue Li, Ming-Jun Sun
Inflammatory bowel disease (IBD) is a type of chronic inflammatory disturbance that affects a number of individuals worldwide; the precise mechanism is unclear and treatment is frequently insufficient to maintain patients in remission. Saccharomyces boulardii is a thermophilic, non‑pathogenic yeast that may be administered for prophylaxis and treatment of a variety of diarrheal diseases. Recent clinical studies have demonstrated that it may have a role in IBD; however, the mechanism of action is unclear...
December 2018: Molecular Medicine Reports
Rui-Gang Hou, Lei Fan, Jun-Jin Liu, Yao Cheng, Zhuang-Peng Chang, Bei Wu, Yun-Yun Shao
The enterohepatic circulation of bile acids (BAs) critically depends on BA transporters and enzymes, which can be affected by inflammatory bowel disease. Diarrhea in colitis is believed to result in part from BA malabsorption. The work aimed to investigate whether diarrhea in colitis was associated with the expression of BA transporters, enzymes, and nuclear receptors. RT-qPCR and Western blot techniques were used to evaluate the gene and protein levels of Cyp7a1, Asbt, SHP, FXR, Ostβ in a 2,4,6-trinitrobenzenesulfonic-acid-induced rat model of colitis...
November 1, 2018: Canadian Journal of Physiology and Pharmacology
Bailey Zwarycz, Adam D Gracz, Kristina R Rivera, Ian A Williamson, Leigh A Samsa, Josh Starmer, Michael A Daniele, Luisa Salter-Cid, Qihong Zhao, Scott T Magness
Background & Aims: Crohn's disease is an inflammatory bowel disease that affects the ileum and is associated with increased cytokines. Although interleukin (IL)6, IL17, IL21, and IL22 are increased in Crohn's disease and are associated with disrupted epithelial regeneration, little is known about their effects on the intestinal stem cells (ISCs) that mediate tissue repair. We hypothesized that ILs may target ISCs and reduce ISC-driven epithelial renewal. Methods: A screen of IL6, IL17, IL21, or IL22 was performed on ileal mouse organoids...
2019: Cellular and Molecular Gastroenterology and Hepatology
Elise Kang, Ali Khalili, Judy Splawski, Thomas J Sferra, Jonathan Moses
Loss of response to anti-tumor necrosis factor (anti-TNF) agents in the treatment of inflammatory bowel disease (IBD) is a major consideration to maintain sustained response. Reversal of immunogenicity can re-establish response and increase the durability of these agents. Strategies to reverse immunogenicity include dose-intensification and/or the addition of an immunomodulator. However, there is a relative paucity of data on the efficacy of such interventions in pediatric IBD patients. Available reports have not strictly utilized homogenous mobility shift assay, which reports on anti-drug antibodies even in the presence of detectable drug, whereas prior studies have been confounded by the use of drug sensitive assays...
October 2018: Pediatric Gastroenterology, Hepatology & Nutrition
Hana Brath, Nishila Mehta, Rachel D Savage, Sudeep S Gill, Wei Wu, Susan E Bronskill, Lynn Zhu, Jerry H Gurwitz, Paula A Rochon
OBJECTIVES: To systematically describe the resources available on preventing, detecting, and reversing prescribing cascades using a scoping review methodology. MEASUREMENTS: We searched Medline, EMBASE, PsychINFO, CINAHL, Cochrane Library, and Sociological Abstracts from inception until July 2017. Other searches (Google Scholar, hand searches) and expert consultations were performed for resources examining how to prevent, detect, or reverse prescribing cascades...
November 2018: Journal of the American Geriatrics Society
Avantika Mishra, Darren N Seril
Biological agents are frequently used in the management of inflammatory bowel disease, and it is important to understand the potential adverse effects of these therapies. Ustekinumab is a human monoclonal antibody that interferes with interleukin-12 and -23 cytokine signaling and is approved for the treatment of moderate to severe Crohn's disease. We report 2 cases of neurological adverse events, one of which is consistent with posterior reversible encephalopathy syndrome (PRES), in the setting of ustekinumab therapy for Crohn's disease...
May 2018: Case Reports in Gastroenterology
Josephine M Ambruzs, Christopher P Larsen
Renal and urinary involvement has been reported to occur in 4% to 23% of inflammatory bowel disease (IBD) patients. Parenchymal renal disease is rare and most commonly affects glomerular and tubulointerstitial compartments. The most common findings on renal biopsy of IBD patients are IgA nephropathy and tubulointerstitial nephritis. Overall morbidity of IBD-related renal manifestations is significant, and there is often only a short window of injury reversibility. This, along with subtle clinical presentation, requires a high index of suspicion and routine monitoring of renal function...
November 2018: Rheumatic Diseases Clinics of North America
Zishuo Wang, Zhenlu Li, Dongcheng Feng, Guo Zu, Yang Li, Yan Zhao, Guangzhi Wang, Shili Ning, Jie Zhu, Feng Zhang, Jihong Yao, Xiaofeng Tian
Intestinal ischemia/reperfusion (I/R)-induced systemic inflammation leads to multiple organ dysfunction syndrome (MODS). Previous studies have indicated that the NLRP3 inflammasome modulates intestinal inflammation; however, the pathophysiological mechanisms remain unclear. Autophagy is a critical metabolic mechanism that promotes cellular survival following ischemic injury. Recently, basal autophagy has been implicated in the alleviation of extensive inflammation. However, the role of autophagy in NLRP3 inflammasome activation in intestinal I/R-induced inflammatory injury remains undefined...
September 13, 2018: Shock
Hazel Tye, Chien-Hsiung Yu, Lisa A Simms, Marcel R de Zoete, Man Lyang Kim, Martha Zakrzewski, Jocelyn S Penington, Cassandra R Harapas, Fernando Souza-Fonseca-Guimaraes, Leesa F Wockner, Adele Preaudet, Lisa A Mielke, Stephen A Wilcox, Yasunori Ogura, Sinead C Corr, Komal Kanojia, Konstantinos A Kouremenos, David P De Souza, Malcolm J McConville, Richard A Flavell, Motti Gerlic, Benjamin T Kile, Anthony T Papenfuss, Tracy L Putoczki, Graham L Radford-Smith, Seth L Masters
Anti-microbial signaling pathways are normally triggered by innate immune receptors when detecting pathogenic microbes to provide protective immunity. Here we show that the inflammasome sensor Nlrp1 aggravates DSS-induced experimental mouse colitis by limiting beneficial, butyrate-producing Clostridiales in the gut. The colitis-protective effects of Nlrp1 deficiency are thus reversed by vancomycin treatment, but recapitulated with butyrate supplementation in wild-type mice. Moreover, an activating mutation in Nlrp1a increases IL-18 and IFNγ production, and decreases colonic butyrate to exacerbate colitis...
September 13, 2018: Nature Communications
Yomna Rashad, Lina Olsson, Anne Israelsson, Åke Öberg, Gudrun Lindmark, Marie-Louise Hammarström, Sten Hammarström, Basel Sitohy
Lymph node metastasis is the most important prognostic characteristic of colorectal cancer. Carcinoembryonic antigen messenger RNA was shown to detect tumor cells that have disseminated to lymph nodes of colorectal cancer patients and to be at least as good as the hematoxylin and eosin method to predict survival in colorectal cancer patients. CXCL17 was recently shown to be ectopically expressed in colon cancer tumors. Therefore, CXCL17 may serve as prognostic marker alone or in combination with carcinoembryonic antigen...
September 2018: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
Yun Ji, Zhaolai Dai, Shiqiang Sun, Xiaoshi Ma, Ying Yang, Patrick Tso, Guoyao Wu, Zhenlong Wu
SCOPE: Inflammatory bowel disease (IBD) is a chronic disease of gastrointestinal tract in which oxidative stress and overactivation of inflammatory response are implicated. The aim of the present study is to test the hypothesis that hydroxyproline (Hyp), an amino acid with an antioxidative property, attenuates dextran sulfate sodium (DSS)-induced colitis in mice. METHODS AND RESULTS: Male C57BL/6 mice supplemented with or without 1% Hyp are subjected to 2.5% DSS in drinking water to induce colitis...
September 5, 2018: Molecular Nutrition & Food Research
C-X Qiao, S Xu, D-D Wang, S-Y Gao, S-F Zhao, M-L Zhang, B Yu, Q Yin, G Zhao
OBJECTIVE: Ulcerative colitis (UC) is an unexplained inflammatory disease in bowel. Some studies reported that microRNA-19b (miR-19b) was closely related to cell inflammatory response. We aimed to explore the molecular mechanism of miR-19b on lipopolysaccharide (LPS)-induced human intestinal cell inflammatory injury. MATERIALS AND METHODS: Caco2 cells were treated with 10 ng/ml LPS to induce inflammatory injury. The expression of miR-19b and runt-related transcription factor 3 (Runx3) was changed in Caco2 cells by cell transfection...
August 2018: European Review for Medical and Pharmacological Sciences
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