67 research outputs found

    Innate and Adaptive Immunity in Inflammatory Bowel Diseases

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    While barrier function and the effects of the intestinal microbiome have only recently moved into the focus of inflammatory bowel disease research, the role of the innate and the adaptive immune system in these gastrointestinal disorders has extensively been studied. Although still not completely understood, the increasing knowledge about the immune system's contribution to the pathophysiology of inflammatory bowel diseases has led to new diagnostic and therapeutic approaches. This review gives a compact overview on this important topic

    Light and sound - emerging imaging techniques for inflammatory bowel disease

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    Mechanisms of Immune Signaling in Colitis-Associated CancerSummary

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    The inflammatory bowel diseases ulcerative colitis and Crohnâs disease are associated with an increased risk for the development of colorectal cancer. During recent years, several immune signaling pathways have been linked to colitis-associated cancer (CAC), largely owing to the availability of suitable preclinical models. Among these, chronic intestinal inflammation has been shown to support tumor initiation through oxidative stressâinduced mutations. A proinflammatory microenvironment that develops, possibly as a result of defective intestinal barrier function and hostâmicrobial interactions, enables tumor promotion. Several molecular pathways such as tumor necrosis factor/nuclear factor-κB or interleukin 6/signal transducer and activator of transcription 3 signaling have been identified as important contributors to CAC development and could be promising therapeutic targets for the prevention and treatment of CAC. Keywords: Colorectal Cancer, Crohn's Disease, Cytokines, Inflammatory Bowel Disease, Interleukin-6, Tumor Necrosis Factor Alpha, Ulcerative Coliti

    Interleukin-6 - A Key Regulator of Colorectal Cancer Development

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    <p>Growing evidence proposes an important role for pro-inflammatory cytokines during tumor development. Several experimental and clinical studies have linked the pleiotropic cytokine interleukin-6 (IL-6) to the pathogenesis of sporadic and inflammation-associated colorectal cancer (CRC). Increased IL-6 expression has been related to advanced stage of disease and decreased survival in CRC patients. According to experimental studies, these effects are mediated through IL-6 trans-signaling promoting tumor cell proliferation and inhibiting apoptosis through gp130 activation on tumor cells with subsequent signaling through Janus kinases (JAKs) and signal transducer and activator of transcription 3 (STAT3).</p><p>During recent years, several therapeutics targeting the IL-6/STAT3 pathway have been developed and pose a promising strategy for the treatment of CRC. This review discusses the molecular mechanisms and possible therapeutic targets involved in IL-6 signaling in CRC.</p
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