Immature myeloid cells, also known as myeloid-derived suppressor cells (MDSCs), include neutrophilic and monocytic myeloid cells, and are found in inflammatory loci and secondary lymphoid organs in mice with intestinal inflammation, inflammatory bowel disease (IBD) patients, and tumor tissues. However, the roles of MDSCs in IBD are not yet well understood, and there are controversies regarding their immunosuppressive functions in IBD. In addition, recent studies have suggested that endoplasmic reticulum (ER) stress in intestinal epithelial cells, especially in Paneth cells, is closely associated with the induction of IBD. However, the ER stress in MDSCs accumulated in the inflamed tissues of IBD patients is not yet fully understood. In the current review, we discuss the presence of accumulated MDSCs in the intestines of IBD patients, and further speculate on their physiological roles in the inflammatory condition with interleukin 17-producing cells, including Th17 cells. In particular, we will discuss the divergent functions of MDSCs in ER stressed intestinal environments, including their pro-inflammatory or immunosuppressive roles, based on the consideration of unfolded protein responses initiated in intestinal epithelial cells by ER stress.

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Imaging of the small bowel is complicated by its length and its overlapping loops. Recently, however, the development of crosssectional imaging techniques, such as computed tomography enterography (CTE) and magnetic resonance enterography (MRE) has shifted fundamental paradigms in the diagnosis and management of patients with suspected or known Crohn's disease (CD). CTE and MRE are noninvasive imaging tests that involve the use of intraluminal oral and intravenous contrast agents to evaluate the small bowel. Here, we review recent advances in each cross-sectional imaging modality, their advantages and disadvantages, and their diagnostic performances in the evaluation of small bowel lesions in CD.

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Crohn's disease (CD) is a disease with chronic inflammation of unknown etiology involving any part of the gastrointestinal tract. The incidence and prevalence of CD are increasing recently in Asia. Half of the CD patients will have intestinal complications, such as strictures or fistulas, within 20 years after diagnosis. Twenty-five percentage of CD patients have had at least one small bowel stricture and 10% have had at least one colonic stricture and lead to significant complications. Most of these patients will require at least one surgery during their lifetime. Early diagnosis and evaluation with adequate managements for the patients can prevent disability and mortality of these patient. Here, we reviewed the current incidence of CD with stricture, the etiology of stricture, and how to diagnose and manage the stricture.

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Epithelial tight junctions (TJs) are the key structures regulating paracellular trafficking of macromolecules. The TJ is multi-protein complex that forms a selective permeable seal between adjacent epithelial cells and demarcates the boundary between apical and basolateral membrane domains. Disruption of the intestinal TJ barrier, followed by permeation of luminal noxious molecules, induces a perturbation of the mucosal immune system and inflammation, which can act as a trigger for the development of intestinal and systemic diseases. Inflammatory bowel disease (IBD) patients demonstrate increased intestinal paracellular permeability. Although it remains unclear whether barrier dysfunction precedes disease or results from active inflammation, increased intestinal TJ disruption is observed in IBD patients suggest that dysregulation of TJ barrier integrity may predispose or enhance IBD progression. Therefore, therapeutic target to restore the TJ barrier integrity may provide effective therapeutic and preventive approaches against IBD. This review discusses the molecular structure and regulation of intestinal TJs and the involvement of intestinal TJs in IBD pathogenesis.

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Life expectancy in Korea has increased, and the number of screening colonoscopies in the elderly has also dramatically increased. The net benefit of colonoscopy in the very elderly (≥80 years of age as defined by the World Health Organization) may be reduced because of the competing risk of mortality due to other diseases. Therefore, the decision to perform screening colonoscopy may be more complex in this age group. As the potential increase in life expectancy due to screening colonoscopy is significantly reduced in the very elderly, this procedure should be limited to those among the very elderly who have substantial life expectancies. Furthermore, considering the common major complications associated with colonoscopy, poor bowel preparation, and the possibility of incomplete colonoscopies in the very elderly, the performance of screening colonoscopy in the very elderly may not be an ideal recommendation. In terms of providing the greatest benefit to the most number of people, patients with the highest potential gain in terms of life expectancy, relative to the diagnostic yield, should be targeted for colonoscopy screening. This review addresses the unique considerations regarding screening colonoscopy in the very elderly and the individualized approach, which involves the weighing of the risks and benefits for each individual with consideration of their overall health status.

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Screening for colorectal cancer (CRC) using sigmoidoscopy or colonoscopy is now common in many developed countries. This concise, evidence-based review looks at the impact of sigmoidoscopy or colonoscopy screening on CRC incidence, CRC mortality and overall mortality. Data from controlled retrospective and prospective (observational or randomized) studies have generally shown that sigmoidoscopy and colonoscopy, whether for diagnostic, screening or surveillance purposes, are associated with a significant reduction in CRC incidence and CRC mortality. The data on their impact on overall mortality is much more limited, with most studies unable to report a reduction in overall mortality. The results of three meta-analyses have confirmed these conclusions. As expected, sigmoidoscopy has a predominant effect on left-sided CRC, although some studies have shown modest effects on right-sided colon cancer as well. Most studies on colonoscopy have demonstrated that the protective effect applies to both right and left-sided cancer, although the protection seemed better on the left side. Despite the introduction of other screening and diagnostic modalities for the colon, such as computed tomography colonography and colonic capsule endoscopy, lower endoscopy will continue to be an important mode of screening for CRC and evaluating the colon.

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Patients with inflammatory bowel disease (IBD) are at an increased risk of developing colorectal cancer (CRC), and key contributing factors include chronic colonic inflammation and the extent and duration of disease. This increase in risk is more likely to result from chronic inflammation of the colonic mucosa than from any clearly defined genetic predisposition. However, globally, the true magnitude of this risk is debatable, since results from different studies are heterogeneous in terms of geographical and methodological variables. The prevalence of IBD-related CRC in the Asia-Pacific region ranges from 0.3% to 1.8% and a recent study found that the cumulative incidence of IBD-related CRC is comparable to that in Western countries. However, the CRC mortality rate in the Asia-Pacific region is on the rise compared with that in Western countries, and a few Asian countries show particularly rapid upward trends in CRC incidence. Although our understanding of the molecular and clinical basis for IBD-related CRC has improved substantially, our means of prevention, endoscopic surveillance, chemoprevention, and prophylactic surgery remain modest at best. Furthermore, published data on IBD-related CRC in the Asia-Pacific region is lacking, and this review addresses many aspects including epidemiology, natural history, etiopathogenesis, morphology, and biological behaviors of IBD-related CRC and sporadic CRC in the Asia-Pacific region. In this review, we will also discuss the risk factors for CRC in IBD patients, endoscopic technology screening, and surveillance programs and management strategies for IBD-related CRC.

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The extensive study of genetic alterations in colorectal cancer (CRC) has led to molecular diagnostics playing an increasingly important role in CRC diagnosis and treatment. Currently, it is believed that CRC is a consequence of the accumulation of both genetic and epigenetic genomic alterations. It is known that there are at least 3 major pathways that lead to colorectal carcinogenesis: (1) the chromosomal instability pathway, (2) the microsatellite instability pathway, and (3) the cytosine-phospho-guanine island methylator phenotype pathway. With recent advances in CRC genetics, the identification of specific molecular alterations responsible for CRC pathogenesis has directly influences clinical care. Patients at high risk for developing CRC can be identified by genetic testing for specific molecular alterations, and the use of molecular biomarkers for predictive and prognostic purposes is also increasing. This is clearly supported by the recent advances in genetic testing for CRC whereby specific molecular alterations are identified for the purpose of guiding treatment with targeting therapies such as anti-endothelial growth factor receptor monoclonal antibodies.

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The incidence and prevalence of inflammatory bowel disease (IBD) in Asia has witnessed a rapid increase within a few decades. The genetic susceptibility and epidemiologic backgrounds in the Asian population have been found to be different from that of Western populations. There is an extensive crosstalk between gut microbiota and human hosts, with evidence of reciprocal interactions. It is well known that gut microbiota can affect the host immune system and in turn, host genetic backgrounds can affect gut microbiota reciprocally. Evidences have implicated gut microbes in the development of IBD, but no causative microorganisms have been identified. Recent advances in sequencing technology and computational analysis have now made identification of complex gut microbiomes accessible. Further research targeting gut microbiota could help in identifying biomarkers to predict clinical response, and therapeutic modalities that might affect their resilience.

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Colonoscopy is currently regarded as the gold standard and preferred screening method for colorectal cancer (CRC). Recently, however, a limitation of colonoscopy in the prevention of CRCs has been identified, particularly in the right-sided colon, and the problem of so-called interval cancers has emerged. The prevalence of interval cancer is estimated to be between 4% and 8% of CRCs detected. Although the exact etiology of interval cancer remains unknown, factors implicated in the development of interval cancers include missed lesions at the time of colonoscopy, incomplete resection of previous neoplastic lesions, different tumor biology, and serrated pathway of carcinogenesis. However, recent evidence suggests that interval cancers are related to the training of the endoscopist and quality of the colonoscopy rather than tumor biology. Therefore, the importance of adequate training and continuous monitoring of the colonoscopy quality, which are amenable to improvement, cannot be overstated in order to prevent the risk of interval cancers. In this study, the current literature regarding the prevalence and potential factors related to interval cancers and colonoscopy quality-related issues are reviewed.

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Natural products have been used as drugs for millennia, and the therapeutic potential of natural products has been studied for more than a century. Since the mid-1880s, approximately 60% of drugs have originated from natural products. Recently, the importance of using natural products has increased, as has interest in discovering efficient new drugs. Natural drugs are desirable for the treatment of inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease. This review discusses the discovery and development of drugs derived from natural products for the treatment of inflammatory bowel diseases.

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Angiogenesis is the formation of new blood vessels from existing ones and an underlying cause of numerous human diseases, including cancer and inflammation. A large body of evidence indicates that angiogenic inhibitors have therapeutic potential in the treatment of vascular diseases. However, detrimental side effects and low efficacy hinder their use in clinical practice. Members of the corticotropin-releasing hormone (CRH) family, which comprises CRH, urocortin I-III, and CRH receptors (CRHR) 1 and 2, are broadly expressed in the brain and peripheral tissues, including the intestine and cardiovascular system. The CRH family regulates stress-related responses through the hypothalamic-pituitary-adrenal axis. Therapeutic agents that target CRH family members offer a new approach to the treatment of various gastrointestinal disorders, including irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and colorectal cancer. Since the discovery that CRHR 2 has anti-angiogenic activity during postnatal development in mice, studies have focused on the role of the CRH system in the modulation of blood vessel formation and cardiovascular function. This review will outline the basic biological functions of the CRH family members and the implications for the development of novel anti-angiogenic therapies.

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Lipopolysaccharide (LPS), a main constituent of Gram-negative bacterial membrane, specifically activates Toll-like receptor 4, leading to the production of pleiotropic cytokines/chemokines which in turn regulate inflammatory and innate and subsequent adaptive immune responses. Given that human gut harbors a large collection of commensal bacteria, LPS released by gut microbes is able to make the great impact on gut homeostasis through the intracellular signaling pathways engaged by host-microbial interaction. Emerging evidence indicates that LPS in the gut has a potency to elicit the pathogenesis of intestinal inflammatory diseases such as inflammatory bowel disease and necrotizing enterocolitis. In this review, we discuss the current understanding of the basic biochemistry of LPS, LPS-induced intracellular signaling, and physiological impacts of LPS in the intestine.

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