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Prof. Yuseok Moon
Laboratory of Mucosal Exposome and Biomodulation, Department of Biomedical Sciences and Biomedical Research Institute, Pusan National University, Yangsan 50612, Korea

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0 Mucosal Immunology
0 mycotoxin
0 intestine
0 ribosome
0 immunotoxicity

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Journal article
Published: 10 May 2021 in Communications Biology
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The majorities of colorectal cancer (CRC) cases are sporadic in origin and a large proportion of etiologies are associated with environmental stress responses. In response to external and internal stress, the ribosome stands sentinel and stress-driven ribosomal dysfunction triggers the cellular decision pathways via transcriptional reprogramming. In the present study, PR domain zinc finger protein (PRDM) 1, a master transcriptional regulator, was found to be closely associated with ribosomal actions in patients with CRC and the murine models. Stress-driven ribosomal dysfunction enhanced PRDM1 levels in intestinal cancer cells, which contributed to their survival and enhanced cancer cell stemness against cancer treatment. Mechanistically, PRDM1 facilitated clustering modulation of insulin-like growth factor (IGF) receptor-associated genes, which supported cancer cell growth and stemness-linked features. Ribosomal dysfunction-responsive PRDM1 facilitated signaling remodeling for the survival of tumor progenitors, providing compelling evidence for the progression of sporadic CRC.

ACS Style

Juil Kim; Yuseok Moon. Mucosal ribosomal stress-induced PRDM1 promotes chemoresistance via stemness regulation. Communications Biology 2021, 4, 1 -14.

AMA Style

Juil Kim, Yuseok Moon. Mucosal ribosomal stress-induced PRDM1 promotes chemoresistance via stemness regulation. Communications Biology. 2021; 4 (1):1-14.

Chicago/Turabian Style

Juil Kim; Yuseok Moon. 2021. "Mucosal ribosomal stress-induced PRDM1 promotes chemoresistance via stemness regulation." Communications Biology 4, no. 1: 1-14.

Journal article
Published: 01 March 2021 in Nutrients
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Despite the beneficial actions of antibiotics against bacterial infections, the use of antibiotics is a crucial etiological factor influencing microbial dysbiosis-associated adverse outcomes in human health. Based on the assumption that gut microbial dysbiosis can provoke behavioral or psychological disorders, the present study evaluated anxiety-linked behavioral changes in a mouse model of streptomycin-induced dysbiosis. Measuring anxiety-like behavior using the light–dark box and elevated plus maze tests indicated that streptomycin treatment caused acute anxiety in mice. As an intervention for dysbiosis-associated distress, the probiotic strain Escherichia coli Nissle 1917 (EcN) was evaluated for its effects on streptomycin-induced behavioral changes in mice. EcN supplementation persistently ameliorated anxiety responses in mice with streptomycin-induced dysbiosis. As an outcome of anxiety, body weight changes were marginally affected by antibiotic treatment. However, mice supplemented with EcN displayed acute retardation of body weight gain, since EcN is known to reduce food intake and increase energy expenditure. Taken together, EcN treatment prominently counteracted streptomycin-induced anxiety in mice, with the metabolically beneficial retardation of body weight gain. The present model simulates psychological disorders in antibiotic users. As a promising intervention, EcN treatment can facilitate psychological relief under conditions of dysbiotic stress by blocking the pathologic gut–brain circuit.

ACS Style

Kiwoong Park; Suhyeon Park; Arulkumar Nagappan; Navin Ray; Juil Kim; Sik Yoon; Yuseok Moon. Probiotic Escherichia coli Ameliorates Antibiotic-Associated Anxiety Responses in Mice. Nutrients 2021, 13, 811 .

AMA Style

Kiwoong Park, Suhyeon Park, Arulkumar Nagappan, Navin Ray, Juil Kim, Sik Yoon, Yuseok Moon. Probiotic Escherichia coli Ameliorates Antibiotic-Associated Anxiety Responses in Mice. Nutrients. 2021; 13 (3):811.

Chicago/Turabian Style

Kiwoong Park; Suhyeon Park; Arulkumar Nagappan; Navin Ray; Juil Kim; Sik Yoon; Yuseok Moon. 2021. "Probiotic Escherichia coli Ameliorates Antibiotic-Associated Anxiety Responses in Mice." Nutrients 13, no. 3: 811.

Review
Published: 11 February 2021 in Journal of Personalized Medicine
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Despite research into the epidemiological link between exposure to particulate matter (PM) and renal disorder, there is limited information available on the etiological complexity and molecular mechanisms. Among the early responsive tissues to PM exposure, the mucosal barrier of the airway and alimentary tract may be a crucial source of pathologic mediators leading to inflammatory renal diseases, including chronic kidney disease (CKD). Given that harmful responses and products in mucosa exposed to PM may enter the circulation and cause adverse outcomes in the kidney, the aim of the present review was to address the impact of PM exposure on the mucosal barrier and the vicious feedback cycle in the mucosal environment. In addition to the PM-induced alteration of mucosal barrier integrity, the microbial community has a pivotal role in the xenobiotic metabolism and individual susceptibility to PM toxicity. The dysbiosis-induced deleterious metabolites of PM and nutrients are introduced systemically via a disrupted mucosal barrier, contributing to renal injuries and pathologic severity. In contrast, the progress of mucosa-associated renal disease is counteracted by endogenous protective responses in the mucosa. Along with direct elimination of the toxic mediators, modulators of the mucosal microbial community should provide a promising platform for mucosa-based personalized interventions against renal disorders caused by air pollution.

ACS Style

Yuseok Moon. Predictive and Preventive Mucosal Communications in Particulate Matter Exposure-Linked Renal Distress. Journal of Personalized Medicine 2021, 11, 118 .

AMA Style

Yuseok Moon. Predictive and Preventive Mucosal Communications in Particulate Matter Exposure-Linked Renal Distress. Journal of Personalized Medicine. 2021; 11 (2):118.

Chicago/Turabian Style

Yuseok Moon. 2021. "Predictive and Preventive Mucosal Communications in Particulate Matter Exposure-Linked Renal Distress." Journal of Personalized Medicine 11, no. 2: 118.

Review
Published: 20 January 2021 in Toxics
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Particulate matter (PM) is a major and the most harmful component of urban air pollution, which may adversely affect human health. PM exposure has been associated with several human diseases, notably respiratory and cardiovascular diseases. In particular, recent evidence suggests that exposure to biomass-derived PM associates with airway inflammation and can aggravate asthma and other allergic diseases. Defective or excess responsiveness in the immune system regulates distinct pathologies, such as infections, hypersensitivity, and malignancies. Therefore, PM-induced modulation of the immune system is crucial for understanding how it causes these diseases and highlighting key molecular mechanisms that can mitigate the underlying pathologies. Emerging evidence has revealed that immune responses to biomass-derived PM exposure are closely associated with the risk of diverse hypersensitivity disorders, including asthma, allergic rhinitis, atopic dermatitis, and allergen sensitization. Moreover, immunological alteration by PM accounts for increased susceptibility to infectious diseases, such as tuberculosis and coronavirus disease-2019 (COVID-19). Evidence-based understanding of the immunological effects of PM and the molecular machinery would provide novel insights into clinical interventions or prevention against acute and chronic environmental disorders induced by biomass-derived PM.

ACS Style

Arulkumar Nagappan; Su Park; Su-Jun Lee; Yuseok Moon. Mechanistic Implications of Biomass-Derived Particulate Matter for Immunity and Immune Disorders. Toxics 2021, 9, 18 .

AMA Style

Arulkumar Nagappan, Su Park, Su-Jun Lee, Yuseok Moon. Mechanistic Implications of Biomass-Derived Particulate Matter for Immunity and Immune Disorders. Toxics. 2021; 9 (2):18.

Chicago/Turabian Style

Arulkumar Nagappan; Su Park; Su-Jun Lee; Yuseok Moon. 2021. "Mechanistic Implications of Biomass-Derived Particulate Matter for Immunity and Immune Disorders." Toxics 9, no. 2: 18.

Hypothesis and theory article
Published: 22 December 2020 in Frontiers in Medicine
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The novel coronavirus disease (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has led to a global pandemic, and resulted in high case-fatality rate in the elderly. In addition to typical respiratory responses, ~50% of clinical cases include gastrointestinal symptoms such as diarrhea, vomiting, abdominal pain, and persistent fecal shedding of the virus even after its clearance from the pulmonary system. In the present study, we assessed aging-associated gut transcriptomic responses considering the gastrointestinal symptoms contributing to COVID-19 severity. Intestinal expression of SARS-CoV-2 receptors and defense biomarkers decreased with increasing age. Moreover, aging-associated integrated stress responses (ISR) and mTOR-linked cell metabolic stress signals counteracted gut defense biomarkers. However, SARS-CoV-2 receptor expression was positively associated with gut barrier integrity potently via downregulation of the two stress-responsive signals. Gut transcriptome-based mechanistic prediction implicates that high susceptibility to COVID-19 in the elderly with low SARS-CoV-2 receptors is due to aging stress-associated defective gut defense, providing a new avenue for viral entry receptor-independent interventions.

ACS Style

Yuseok Moon. Public Database-Driven Insights Into Aging Stress-Associated Defective Gut Barrier With Low SARS-CoV-2 Receptors. Frontiers in Medicine 2020, 7, 606991 .

AMA Style

Yuseok Moon. Public Database-Driven Insights Into Aging Stress-Associated Defective Gut Barrier With Low SARS-CoV-2 Receptors. Frontiers in Medicine. 2020; 7 ():606991.

Chicago/Turabian Style

Yuseok Moon. 2020. "Public Database-Driven Insights Into Aging Stress-Associated Defective Gut Barrier With Low SARS-CoV-2 Receptors." Frontiers in Medicine 7, no. : 606991.

Original research article
Published: 16 July 2020 in Frontiers in Immunology
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Type B 8-keto-trichothecenes are muco-active mycotoxins that exist as inevitable contaminants in cereal-based foodstuffs. Gut-associated inflammation is an early frontline response during human and animal exposure to these mycotoxins. Despite various tools for chemical identification, optimized biomonitoring of sentinel response-associated biomarkers is required to assess the specific proinflammatory actions of 8-keto-trichothecenes in the gut epithelial barrier. In the present study, intoxication with 8-keto-trichothecenes in human intestinal epithelial cells was found to trigger early response gene 1 product (EGR-1) that plays crucial roles in proinflammatory chemokine induction. In contrast, epithelial exposure to 8-keto-trichothecenes resulted in downregulated expression of nuclear factor NF-kappa-B p65 protein, a key transcription factor, during general inflammatory responses in the gut. Based on the early molecular patterns of expression, the inflammation-inducing activity of 8-keto-trichothecenes was quantified using intestinal epithelial cells with dual reporters for EGR-1 and p65 proteins. EGR-1-responsive elements were linked to luciferase reporter while p65 promoter was bound to secretory alkaline phosphatase (SEAP) reporter. In response to conventional inflammagens such as endotoxins and cytokines such as TNF-α, both luciferase and SEAP activity were elevated in a dose-dependent manner. However, as expected from the mechanistic evaluation, 8-keto-trichothecene-exposed dual reporters of luciferase and SEAP displayed contrasting expression patterns. Furthermore, 8-keto-trichothecene-elevated EGR-1-responsive luciferase activity was improved by deficiency of PSMA3, an α-type subunit of the 20S proteasome core complex for ubiquitin-dependent EGR-1 degradation. This molecular event-based dual biomonitoring in epithelial cells is a promising supplementary tool for detecting typical molecular inflammatory pathways in response to 8-keto-trichothecenes in the food matrix.

ACS Style

Seong-Hwan Park; Yuseok Moon. Enterocyte-Based Bioassay via Quantitative Combination of Proinflammatory Sentinels Specific to 8-keto-trichothecenes. Frontiers in Immunology 2020, 11, 1530 .

AMA Style

Seong-Hwan Park, Yuseok Moon. Enterocyte-Based Bioassay via Quantitative Combination of Proinflammatory Sentinels Specific to 8-keto-trichothecenes. Frontiers in Immunology. 2020; 11 ():1530.

Chicago/Turabian Style

Seong-Hwan Park; Yuseok Moon. 2020. "Enterocyte-Based Bioassay via Quantitative Combination of Proinflammatory Sentinels Specific to 8-keto-trichothecenes." Frontiers in Immunology 11, no. : 1530.

Journal article
Published: 27 May 2020 in Communications Biology
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In response to internal and external insults, the intestinal lining undergoes various types of epithelial adaptation or pathologic distress via stress-responsive eIF2α kinase signaling and subsequent cellular reprogramming. As a vital platform for growth factor-linked adaptive signaling, caveolae were evaluated for epithelial modulation of the insulted gut. Patients under ulcerative insult displayed enhanced expression of caveolin-1, the main structural component of caveolae, which was positively associated with expression of protein kinase R (PKR), the ribosomal stress-responsive eIF2α kinase. PKR-linked biological responses were simulated in experimental gut models of ribosome-inactivating stress using mice and Caenorhabditis elegans. Caveolar activation counteracted the expression of wound-protective epidermal growth factor receptor (EGFR) and its target genes, such as chemokines that were pivotal for epithelial integrity in the ribosome-inactivated gut. Mechanistic findings regarding ribosomal inactivation-associated disorders in the gut barrier provide crucial molecular evidence for detrimental caveolar actions against EGFR-mediated epithelial protection in patients with IBD.

ACS Style

Seong-Hwan Park; Juil Kim; Yuseok Moon. Caveolar communication with xenobiotic-stalled ribosomes compromises gut barrier integrity. Communications Biology 2020, 3, 1 -18.

AMA Style

Seong-Hwan Park, Juil Kim, Yuseok Moon. Caveolar communication with xenobiotic-stalled ribosomes compromises gut barrier integrity. Communications Biology. 2020; 3 (1):1-18.

Chicago/Turabian Style

Seong-Hwan Park; Juil Kim; Yuseok Moon. 2020. "Caveolar communication with xenobiotic-stalled ribosomes compromises gut barrier integrity." Communications Biology 3, no. 1: 1-18.

Journal article
Published: 01 May 2020 in iScience
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Stress-driven ribosome dysfunction triggers an eIF2α-mediated integrated stress response to maintain cellular homeostasis. Among four key eIF2α kinases, protein kinase R (PKR) expression positively associates with poor prognoses for colorectal cancer (CRC) patients. We identified PKR-linked Wnt signaling networks that facilitate early inflammatory niche and epithelial-mesenchymal transitions of tumor tissues in response to ribosomal insults. However, the downstream Wnt signaling target fibrogenic connective tissue growth factor (CTGF/CCN2) regulates the nuclear translocation of β-catenin in a negative feedback manner. Moreover, dwindling expression of the Wnt/β-catenin pathway-regulator CTGF triggers noncanonical Wnt pathway-mediated exacerbation of intestinal cancer progression such as an increase in cancer stemness and acquisition of chemoresistance in the presence of ribosomal insults. The Wnt-CTGF-circuit-associated landscape of oncogenic signaling events was verified with clinical genomic profiling. This ribosome-associated wave of crosstalk between stress and oncogenes provides valuable insight into potential molecular interventions against intestinal malignancies.

ACS Style

Ki Hyung Kim; Seung Joon Lee; Juil Kim; Yuseok Moon. Dynamic Malignant Wave of Ribosome-Insulted Gut Niche via the Wnt-CTGF/CCN2 Circuit. iScience 2020, 23, 101076 .

AMA Style

Ki Hyung Kim, Seung Joon Lee, Juil Kim, Yuseok Moon. Dynamic Malignant Wave of Ribosome-Insulted Gut Niche via the Wnt-CTGF/CCN2 Circuit. iScience. 2020; 23 (5):101076.

Chicago/Turabian Style

Ki Hyung Kim; Seung Joon Lee; Juil Kim; Yuseok Moon. 2020. "Dynamic Malignant Wave of Ribosome-Insulted Gut Niche via the Wnt-CTGF/CCN2 Circuit." iScience 23, no. 5: 101076.

Original paper
Published: 30 September 2019 in Molecular & Cellular Toxicology
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Heavy metals affect various processes in the embryonic development. Embryonic fibroblasts (EFs) play key roles in the innate recognition and wound healing in reproductive tissues. Based on the relative toxicities of different inorganic metals and inorganic nonmetallic compounds against murine and chicken EF cells, mechanistic estimations were performed based on transcriptomic analyses. Lead (II) acetate induced preferential injuries in the chicken EF and mechanistic analyses using transcriptome revealed that chemokine receptor-associated events are potently involved in metal-induced adverse actions. As an early sentinel of metal exposure, the precision-cut intestine slices (PCIS) induced the expression of chemokines including CXCLi1 or CXCLi2, which were potent gut-derived factors that activate chemokine receptors in reproductive organs after circulation. EF-selective metals can be estimated to trigger the chemokine circuit in the gut-reproductive axis of chickens. This in vitro methodology using PCIS-EF culture could be used as a promising alternate platform for the reproductive immunotoxicological assessment.

ACS Style

Ki Hyung Kim; Juil Kim; Jae Yong Han; Yuseok Moon. In vitro estimation of metal-induced disturbance in chicken gut-oviduct chemokine circuit. Molecular & Cellular Toxicology 2019, 15, 443 -452.

AMA Style

Ki Hyung Kim, Juil Kim, Jae Yong Han, Yuseok Moon. In vitro estimation of metal-induced disturbance in chicken gut-oviduct chemokine circuit. Molecular & Cellular Toxicology. 2019; 15 (4):443-452.

Chicago/Turabian Style

Ki Hyung Kim; Juil Kim; Jae Yong Han; Yuseok Moon. 2019. "In vitro estimation of metal-induced disturbance in chicken gut-oviduct chemokine circuit." Molecular & Cellular Toxicology 15, no. 4: 443-452.

Journal article
Published: 08 September 2019 in Nutrients
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The epithelial barrier is the frontline defense against enteropathogenic bacteria and nutrition-linked xenobiotic stressors in the alimentary tract. In particular, enteropathogenic Escherichia coli (EPEC) insults the gut barrier and is increasingly implicated in chronic intestinal diseases such as inflammatory bowel disease. For the efficient development of intervention against barrier-linked distress, the present study provided a Caenorhabditis elegans-based assessment instead of extensive preclinical evaluations using mammalian models. In particular, EPEC infected the gut and shortened the lifespan of C. elegans, which was counteracted by colonization of E. coli strain Nissle 1917 (EcN). In addition to the competitive actions of EcN against EPEC, EcN improved the gut barrier integrity of worms via the Zonula occludens ortholog (Zoo-1) induction, which was verified in the murine infection and colitis model. The worm-based assessment provided a crucial methodology and important insights into the potent chronic events in the human gut barrier after the ingestion of probiotic candidates as a mucoactive dietary or therapeutic agent.

ACS Style

Juil Kim; Yuseok Moon. Worm-Based Alternate Assessment of Probiotic Intervention against Gut Barrier Infection. Nutrients 2019, 11, 2146 .

AMA Style

Juil Kim, Yuseok Moon. Worm-Based Alternate Assessment of Probiotic Intervention against Gut Barrier Infection. Nutrients. 2019; 11 (9):2146.

Chicago/Turabian Style

Juil Kim; Yuseok Moon. 2019. "Worm-Based Alternate Assessment of Probiotic Intervention against Gut Barrier Infection." Nutrients 11, no. 9: 2146.

Journal article
Published: 22 August 2019 in JCI Insight
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Although mucoactive proteins, such as epidermal growth factor (EGF), could improve clinical outcomes of intestinal ulcerative diseases, their gastrointestinal application is limited because of their proteolytic digestion or concerns about tumor promotion. In the present study, ATP-binding cassette (ABC) transporter–linked secretion of human EGF from probiotic Escherichia coli (EGF-EcN) was created to promote beneficial actions of the EGF receptor, which is notably attenuated in patients with intestinal ulcerative injuries. Preventive and postinjury treatment with EGF-EcN alleviated intestinal ulcers and other readouts of disease severity in murine intestinal ulcer models. EGF-EcN administration promoted the restitutive recovery of damaged epithelial layers, particularly via upward expansion of highly proliferating progenitor cells from the lower crypts. Along with the epithelial barrier benefit, EGF-EcN improved goblet cell–associated mucosal integrity, which controls the access of luminal microbiota to the underlying host tissues. Despite concern about the oncogenic action of EGF, EGF-EcN did not aggravate colitis-associated colon cancer; instead, it alleviated protumorigenic activities and improved barrier integrity in the lesions. All findings indicate that probiotic bacteria–based precision delivery of human EGF is a promising mucosal intervention against gastrointestinal ulcers and malignant distress through crypt-derived barrier restoration.

ACS Style

Mira Yu; Juil Kim; Jung Hoon Ahn; Yuseok Moon. Nononcogenic restoration of the intestinal barrier by E. coli–delivered human EGF. JCI Insight 2019, 4, 1 .

AMA Style

Mira Yu, Juil Kim, Jung Hoon Ahn, Yuseok Moon. Nononcogenic restoration of the intestinal barrier by E. coli–delivered human EGF. JCI Insight. 2019; 4 (16):1.

Chicago/Turabian Style

Mira Yu; Juil Kim; Jung Hoon Ahn; Yuseok Moon. 2019. "Nononcogenic restoration of the intestinal barrier by E. coli–delivered human EGF." JCI Insight 4, no. 16: 1.

Review
Published: 10 May 2019 in Nutrients
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Although hereditary hemochromatosis is associated with the mutation of genes involved in iron transport and metabolism, secondary hemochromatosis is due to external factors, such as intended or unintended iron overload, hemolysis-linked iron exposure or other stress-impaired iron metabolism. The present review addresses diet-linked etiologies of hemochromatosis and their pathogenesis in the network of genes and nutrients. Although the mechanistic association to diet-linked etiologies can be complicated, the stress sentinels are pivotally involved in the pathological processes of secondary hemochromatosis in response to iron excess and other external stresses. Moreover, the mutations in these sentineling pathway-linked genes increase susceptibility to secondary hemochromatosis. Thus, the crosstalk between nutrients and genes would verify the complex procedures in the clinical outcomes of secondary hemochromatosis and chronic complications, such as malignancy. All of this evidence provides crucial insights into comprehensive clinical or nutritional interventions for hemochromatosis.

ACS Style

Chang-Kyu Oh; Yuseok Moon. Dietary and Sentinel Factors Leading to Hemochromatosis. Nutrients 2019, 11, 1047 .

AMA Style

Chang-Kyu Oh, Yuseok Moon. Dietary and Sentinel Factors Leading to Hemochromatosis. Nutrients. 2019; 11 (5):1047.

Chicago/Turabian Style

Chang-Kyu Oh; Yuseok Moon. 2019. "Dietary and Sentinel Factors Leading to Hemochromatosis." Nutrients 11, no. 5: 1047.

Journal article
Published: 28 March 2019 in Microbiology and Biotechnology Letters
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ACS Style

Juil Kim; Joongkon Kim; Mira Yu; Yuseok Moon. Structural Disorganization of Intestinal Tumor Spheroid by Microbial Ribotoxins. Microbiology and Biotechnology Letters 2019, 47, 164 -171.

AMA Style

Juil Kim, Joongkon Kim, Mira Yu, Yuseok Moon. Structural Disorganization of Intestinal Tumor Spheroid by Microbial Ribotoxins. Microbiology and Biotechnology Letters. 2019; 47 (1):164-171.

Chicago/Turabian Style

Juil Kim; Joongkon Kim; Mira Yu; Yuseok Moon. 2019. "Structural Disorganization of Intestinal Tumor Spheroid by Microbial Ribotoxins." Microbiology and Biotechnology Letters 47, no. 1: 164-171.

Original research article
Published: 23 February 2018 in Frontiers in Immunology
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Adlay is a cereal crop that has long been used as traditional herbal medicine and as a highly nourishing food. However, deoxynivalenol (DON), the most prevalent trichothecene mycotoxin worldwide, frequently spoils grains, including adlay, via fungal infection. On the basis of an assumption that the actions of DON in the gut could be modified by adlay consumption, we simulated the impacts of co-exposure in enterocytes and investigated the effectiveness of treatment with adlay for reducing the risk of DON-induced inflammation and epithelia barrier injury. In particular, adlay suppressed DON-induced pro-inflammatory signals such as mitogen-activated kinase transduction and the epidermal growth factor receptor-linked pathway. In addition to regulation of pro-inflammatory responses, adlay treatment interfered with DON-induced disruption of the epithelial barrier. Mechanistically, adlay could boost the activation of protein kinase C (PKC) and cytosolic translocation of human antigen R (HuR) protein, which played critical roles in the epithelial restitution, resulting in protection against disruption of enterocyte barrier integrity. Notably, DON abrogated the Ras homolog gene family member A GTPase-mediated actin cytoskeletal network, which was diminished by adlay treatment in PKC and HuR-dependent ways. Taken together, this study provides evidences for adlay-based attenuation of trichothecene-induced gut distress, implicating potential use of a new gut protector against enteropathogenic insults in diets.

ACS Style

Zhimin Du; Ki Hyung Kim; Juil Kim; Yuseok Moon. Fungal Deoxynivalenol-Induced Enterocyte Distress Is Attenuated by Adulterated Adlay: In Vitro Evidences for Mucoactive Counteraction. Frontiers in Immunology 2018, 9, 186 .

AMA Style

Zhimin Du, Ki Hyung Kim, Juil Kim, Yuseok Moon. Fungal Deoxynivalenol-Induced Enterocyte Distress Is Attenuated by Adulterated Adlay: In Vitro Evidences for Mucoactive Counteraction. Frontiers in Immunology. 2018; 9 ():186.

Chicago/Turabian Style

Zhimin Du; Ki Hyung Kim; Juil Kim; Yuseok Moon. 2018. "Fungal Deoxynivalenol-Induced Enterocyte Distress Is Attenuated by Adulterated Adlay: In Vitro Evidences for Mucoactive Counteraction." Frontiers in Immunology 9, no. : 186.

Review
Published: 01 July 2017 in Pharmacological Research
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In spite of the beneficial actions of non-steroid anti-inflammatory drugs (NSAIDs) in epithelial inflammation and cancers, their use is limited because of their cyclooxygenase-dependent or independent gastrointestinal toxicity. As an eicosanoid-independent mediator, NSAID-activated gene 1 (NAG-1) has been assessed for its involvement in cellular integrity and pathogenesis in mucosal inflammation and carcinogenesis. At the cellular levels, NAG-1 is involved in the cell growth regulation (cell death, cell cycle arrest, or proliferation) in epithelial and mesenchymal tissues. Moreover, NAG-1 can modulate inflammatory responses in either direct or indirect manner, which ultimately affects fibrogenic and tumorigenic processes in various disease states. Finally, NAG-1 has been assessed for its contribution to cellular behavior, such as the mobility of epithelial and malignant cells in response to the external insults or oncogenic stimulation in the mucosa. This review on the "Yin-Yang" nature of NAG-1-mediated responses provides comprehensive insights into therapeutic and diagnostic interventions for mucosal health and integrity in the human body.

ACS Style

Yuseok Moon. NSAID-activated gene 1 and its implications for mucosal integrity and intervention beyond NSAIDs. Pharmacological Research 2017, 121, 122 -128.

AMA Style

Yuseok Moon. NSAID-activated gene 1 and its implications for mucosal integrity and intervention beyond NSAIDs. Pharmacological Research. 2017; 121 ():122-128.

Chicago/Turabian Style

Yuseok Moon. 2017. "NSAID-activated gene 1 and its implications for mucosal integrity and intervention beyond NSAIDs." Pharmacological Research 121, no. : 122-128.

Journal article
Published: 01 February 2017 in Toxicology in Vitro
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Deoxynivalenol (DON), the most prevalent mycotoxin worldwide, leads to economic losses for animal food production. Swine is a most sensitive domestic animal to DON due to rapid absorption and low detoxification by gut microbiota. Specifically, DON can severely damage pig intestinal tissue by disrupting the intestinal barrier and inducing inflammatory responses. We evaluated the effects of several mycotoxin detoxifiers including bentonites, yeast cell wall components, and mixture-typed detoxifier composed of mineral, microorganisms, and phytogenic substances on DON-insulted intestinal barrier and pro-inflammatory responses using in vitro porcine enterocyte culture model. DON-induced disruption of the in vitro gut barrier was attenuated by all three mycotoxin detoxifiers in dose-dependent manners. These mycotoxin detoxifiers also suppressed DON-induced pro-inflammatory chemokine expression to different degrees, which was mediated by downregulation of mitogen-activated kinases and early growth response-1. Of note, the mixture-typed detoxifier was the most prominent mitigating agent at the cellular levels whereas the high dose of bentonite clay also had suppressive action against DON-induced pro-inflammatory insult. The in vitro porcine enterocyte-based assessment of intestinal barrier integrity and inflammatory signals provides sensitive and simplified alternative bioassay of feed additives such as detoxifiers against enteropathogenic mycotoxins with comprehensive mechanistic confirmation.

ACS Style

Seong-Hwan Park; Juil Kim; Dongwook Kim; Yuseok Moon. Mycotoxin detoxifiers attenuate deoxynivalenol-induced pro-inflammatory barrier insult in porcine enterocytes as an in vitro evaluation model of feed mycotoxin reduction. Toxicology in Vitro 2017, 38, 108 -116.

AMA Style

Seong-Hwan Park, Juil Kim, Dongwook Kim, Yuseok Moon. Mycotoxin detoxifiers attenuate deoxynivalenol-induced pro-inflammatory barrier insult in porcine enterocytes as an in vitro evaluation model of feed mycotoxin reduction. Toxicology in Vitro. 2017; 38 ():108-116.

Chicago/Turabian Style

Seong-Hwan Park; Juil Kim; Dongwook Kim; Yuseok Moon. 2017. "Mycotoxin detoxifiers attenuate deoxynivalenol-induced pro-inflammatory barrier insult in porcine enterocytes as an in vitro evaluation model of feed mycotoxin reduction." Toxicology in Vitro 38, no. : 108-116.

Journal article
Published: 01 February 2017 in Microbes and Infection
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NSAID-activated Gene 1 (NAG-1) is a prognostic indicator of chronic inflammatory diseases and aggressive tumors. Among the stress sentinels in response to infection by enteropathogenic Escherichia coli (EPEC) or other pathogenic E. coli, C/EBP homologous protein (CHOP), a representative stress-regulated transcription factor, was prominently increased and assessed for its involvement in NAG-1-mediated pathogenic cellular responses. NAG-1 expression was transcriptionally upregulated by CHOP, which promoted chemokine production through sustained NF-κB activation. Mechanistically, NF-κB activation by NAG-1 was due to TGFβ-activated kinase 1 (TAK-1)-mediated pathway rather than SMAD-associated signals. Moreover, CHOP and subsequent TAK-1-linked signals were also involved in bacterial invasion into human cells. Therefore, CHOP as an infection-induced sentinel played crucial roles in induction of NAG-1 and subsequent prolonged activation of pro-inflammatory responses to EPEC infection or related chronic pathogenic states.

ACS Style

Seong-Hwan Park; Mira Yu; Juil Kim; Yuseok Moon. C/EBP homologous protein promotes NSAID-activated gene 1-linked pro-inflammatory signals and enterocyte invasion by enteropathogenic Escherichia coli. Microbes and Infection 2017, 19, 110 -121.

AMA Style

Seong-Hwan Park, Mira Yu, Juil Kim, Yuseok Moon. C/EBP homologous protein promotes NSAID-activated gene 1-linked pro-inflammatory signals and enterocyte invasion by enteropathogenic Escherichia coli. Microbes and Infection. 2017; 19 (2):110-121.

Chicago/Turabian Style

Seong-Hwan Park; Mira Yu; Juil Kim; Yuseok Moon. 2017. "C/EBP homologous protein promotes NSAID-activated gene 1-linked pro-inflammatory signals and enterocyte invasion by enteropathogenic Escherichia coli." Microbes and Infection 19, no. 2: 110-121.

Journal article
Published: 30 November 2016 in Journal of Life Science
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Comparative Evaluation of Colon Cancer Stemness and Chemoresistance in Optimally Constituted HCT-8 cell-based Spheroids Cancer stem cell;chemoresistance;colon cancer;5-Fluorouracil (5-FU);spheroid; Cancer is a complex disease heterogeneously composed of various types of cells including cancer stem-like cells responsible for relapse and chemoresistance in the tumor microenvironment. The conventional two-dimensional cell culture-based platform has critical limitations for representing the heterogeneity of cancer cells in the three-dimensional tumor niche in vivo. To overcome this insufficiency, three-dimensional cell culture methods in a scaffold-dependent or -free physical environment have been developed. In this study, we improved and simplified the HCT-8 colon cancer cell-based spheroid culture protocol and evaluated the relationship between cancer stemness and responses of chemosensitivity to 5- Fluorouracil (5-FU), a representative anticancer agent against colon cancer. Supplementation with defined growth factors in the medium and the culture dish of the regular surface with low attachment were required for the formation of constant-sized spheroids containing $CD44^+$ and $CD133^+$ colon cancer stem cells. The chemo-sensitivities of $CD44^+$ cancer stem cells in the spheroids were much lower than those of $CD44^-$ non-stem-like cancer cells, indicating that the chemoresistance to 5-FU is due to the stemness of colon cancer cells. Taken together, the inflammation and oncogenic gut environment-sensitive HCT-8 cell-based colon cancer spheroid culture and comparative evaluation using the simplified model would be an efficient and applicable way to estimate colon cancer stemness and pharmaceutical response to anticancer drugs in the realistic tumor niche.

ACS Style

Seung Joon Lee; Hyoung-Kab Kim; Hyang Burm Lee; Yuseok Moon. Comparative Evaluation of Colon Cancer Stemness and Chemoresistance in Optimally Constituted HCT-8 cell-based Spheroids. Journal of Life Science 2016, 26, 1313 -1319.

AMA Style

Seung Joon Lee, Hyoung-Kab Kim, Hyang Burm Lee, Yuseok Moon. Comparative Evaluation of Colon Cancer Stemness and Chemoresistance in Optimally Constituted HCT-8 cell-based Spheroids. Journal of Life Science. 2016; 26 (11):1313-1319.

Chicago/Turabian Style

Seung Joon Lee; Hyoung-Kab Kim; Hyang Burm Lee; Yuseok Moon. 2016. "Comparative Evaluation of Colon Cancer Stemness and Chemoresistance in Optimally Constituted HCT-8 cell-based Spheroids." Journal of Life Science 26, no. 11: 1313-1319.

Journal article
Published: 01 November 2016 in Journal of Biological Chemistry
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Patients with chronic intestinal ulcerative diseases, such as inflammatory bowel disease, tend to exhibit abnormal lipid profiles, which may affect the gut epithelial integrity. We hypothesized that epithelial cholesterol depletion may trigger inflammation-checking machinery via cholesterol sentinel signaling molecules whose disruption in patients may aggravate inflammation and disease progression. In the present study, sterol regulatory element-binding protein 2 (SREBP2) as the cholesterol sentinel was assessed for its involvement in the epithelial inflammatory responses in cholesterol-depleted enterocytes. Patients and experimental animals with intestinal ulcerative injuries showed suppression in epithelial SREBP2. Moreover, SREBP2-deficient enterocytes showed enhanced pro-inflammatory signals in response to inflammatory insults, indicating regulatory roles of SREBP2 in gut epithelial inflammation. However, epithelial cholesterol depletion transiently induced pro-inflammatory chemokine expression regardless of the well known pro-inflammatory nuclear factor-κB signals. In contrast, cholesterol depletion also exerts regulatory actions to maintain epithelial homeostasis against excessive inflammation via SREBP2-associated signals in a negative feedback loop. Mechanistically, SREBP2 and its induced target EGR-1 were positively involved in induction of peroxisome proliferator-activated receptor γ (PPARγ), a representative anti-inflammatory transcription factor. As a crucial target of the SREBP2-EGR-1-PPARγ-associated signaling pathways, the mRNA stabilizer, human antigen R (HuR) was retained in nuclei, leading to reduced stability of pro-inflammatory chemokine transcripts. This mechanistic investigation provides clinical insights into protective roles of the epithelial cholesterol deficiency against excessive inflammatory responses via the SREBP2-HuR circuit, although the deficiency triggers transient pro-inflammatory signals.

ACS Style

Seong-Hwan Park; Juil Kim; Mira Yu; Jae-Hong Park; Yong Sik Kim; Yuseok Moon. Epithelial Cholesterol Deficiency Attenuates Human Antigen R-linked Pro-inflammatory Stimulation via an SREBP2-linked Circuit. Journal of Biological Chemistry 2016, 291, 24641 -24656.

AMA Style

Seong-Hwan Park, Juil Kim, Mira Yu, Jae-Hong Park, Yong Sik Kim, Yuseok Moon. Epithelial Cholesterol Deficiency Attenuates Human Antigen R-linked Pro-inflammatory Stimulation via an SREBP2-linked Circuit. Journal of Biological Chemistry. 2016; 291 (47):24641-24656.

Chicago/Turabian Style

Seong-Hwan Park; Juil Kim; Mira Yu; Jae-Hong Park; Yong Sik Kim; Yuseok Moon. 2016. "Epithelial Cholesterol Deficiency Attenuates Human Antigen R-linked Pro-inflammatory Stimulation via an SREBP2-linked Circuit." Journal of Biological Chemistry 291, no. 47: 24641-24656.

Journal article
Published: 27 October 2016 in Toxins
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Adlay seed samples were collected from three adlay growing regions (Yeoncheon, Hwasun, and Eumseong region) in Korea during 2012. Among all the samples collected, 400 seeds were tested for fungal occurrence by standard blotter and test tube agar methods and different taxonomic groups of fungal genera were detected. The most predominant fungal genera encountered were Fusarium, Phoma, Alternaria, Cladosporium, Curvularia, Cochliobolus and Leptosphaerulina. Fusarium species accounted for 45.6% of all species found; and, with phylogenetic analysis based on the combined sequences of two protein coding genes (EF-1α and β-tubulin), 10 Fusarium species were characterized namely, F. incarnatum (11.67%), F. kyushuense (10.33%), F. fujikuroi (8.67%), F. concentricum (6.00%), F. asiaticum (5.67%), F. graminearum (1.67%), F. miscanthi (0.67%), F. polyphialidicum (0.33%), F. armeniacum (0.33%), and F. thapsinum (0.33%). The Fusarium species were then examined for their morphological characteristics to confirm their identity. Morphological observations of the species correlated well with and confirmed their molecular identification. The ability of these isolates to produce the mycotoxins fumonisin (FUM) and zearalenone (ZEN) was tested by the ELISA quantitative analysis method. The result revealed that FUM was produced only by F. fujikuroi and that ZEN was produced by F. asiaticum and F. graminearum.

ACS Style

Tae Jin An; Kyu Seop Shin; Narayan Chandra Paul; Young Guk Kim; Seon Woo Cha; Yuseok Moon; Seung Hun Yu; Sang-Keun Oh. Prevalence, Characterization, and Mycotoxin Production Ability of Fusarium Species on Korean Adlay (Coix lacrymal-jobi L.) Seeds. Toxins 2016, 8, 310 .

AMA Style

Tae Jin An, Kyu Seop Shin, Narayan Chandra Paul, Young Guk Kim, Seon Woo Cha, Yuseok Moon, Seung Hun Yu, Sang-Keun Oh. Prevalence, Characterization, and Mycotoxin Production Ability of Fusarium Species on Korean Adlay (Coix lacrymal-jobi L.) Seeds. Toxins. 2016; 8 (11):310.

Chicago/Turabian Style

Tae Jin An; Kyu Seop Shin; Narayan Chandra Paul; Young Guk Kim; Seon Woo Cha; Yuseok Moon; Seung Hun Yu; Sang-Keun Oh. 2016. "Prevalence, Characterization, and Mycotoxin Production Ability of Fusarium Species on Korean Adlay (Coix lacrymal-jobi L.) Seeds." Toxins 8, no. 11: 310.