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Journal articles on the topic 'Gastroenterology; Mucosal immunology'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

McGowan, Ian, Anthony Chalmers, Graham-Radford Smith, and Derek Jewell. "ADVANCES IN MUCOSAL IMMUNOLOGY." Gastroenterology Clinics of North America 26, no. 2 (June 1997): 145–73. http://dx.doi.org/10.1016/s0889-8553(05)70291-0.

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2

Kao, John Y. "Principles of Mucosal Immunology." Gastroenterology 145, no. 2 (August 2013): 483. http://dx.doi.org/10.1053/j.gastro.2013.06.013.

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3

MacDonald, T. T. "Essentials of Mucosal Immunology." Gut 40, no. 3 (March 1, 1997): 432–33. http://dx.doi.org/10.1136/gut.40.3.432-b.

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4

Fiocchi, Claudio. "Handbook of mucosal immunology." Gastroenterology 107, no. 3 (September 1994): 901–2. http://dx.doi.org/10.1016/0016-5085(94)90153-8.

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5

MACPHERSON, A. J. S. "Mucosal T cells. Chemical Immunology. Vol 71." Gut 47, no. 1 (July 1, 2000): 157. http://dx.doi.org/10.1136/gut.47.1.157.

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6

Abreu, Maria T. "Updates in mucosal immunology for inflammatory bowel diseases." Current Opinion in Gastroenterology 34, no. 6 (November 2018): 375–76. http://dx.doi.org/10.1097/mog.0000000000000484.

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7

Rescigno, Maria. "Mucosal immunology and bacterial handling in the intestine." Best Practice & Research Clinical Gastroenterology 27, no. 1 (February 2013): 17–24. http://dx.doi.org/10.1016/j.bpg.2013.03.004.

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8

Naito, Yuji. "45th Scientific Meeting of the Japanese Society for Mucosal Immunology." Digestion 78, no. 2-3 (2008): 103–12. http://dx.doi.org/10.1159/000172963.

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9

Buchner, Anna M. "Confocal Laser Endomicroscopy in the Evaluation of Inflammatory Bowel Disease." Inflammatory Bowel Diseases 25, no. 8 (March 16, 2019): 1302–12. http://dx.doi.org/10.1093/ibd/izz021.

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Abstract Inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis, can be effectively monitored with the use of endoscopy. The additional application of small field imaging technology such as confocal laser endomicroscopy CLE during ongoing endoscopic evaluation has led to real-time visualization of mucosal abnormalities and thus in vivo histology. The endomicroscopy (CLE) can improve IBD endoscopic evaluation by identifying seemingly normal-appearing mucosa, assessing the function of the intestinal barrier of the epithelium and vascular permeability, and by characterizing any mucosal lesions, including dysplastic lesions. CLE used during conventional endoscopy could especially facilitate the evaluation of mucosal healing in IBD. In addition, future developments in molecular imaging in IBD may optimize therapeutic approaches by identifying mucosal targets for therapy and determining the reasons for lack of response to specific therapy or subsequent loss of the response.

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Liang, Tony, Leonard Presta, Jennifer Brazil, Charles Parkos, and Jennifer Cheng. "VALIDATION OF HPTM-001, A HUMANIZED CANDIDATE THERAPEUTIC ANTIBODY FOR PROMOTING MUCOSAL WOUND HEALING IN IBD." Inflammatory Bowel Diseases 27, Supplement_1 (January 1, 2021): S37. http://dx.doi.org/10.1093/ibd/izaa347.090.

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Abstract A hallmark of the clinical course of patients with Inflammatory Bowel Disease (IBD) is poorly healing erosions and ulcers in the intestinal mucosa. Despite the adverse clinical consequences of non-healing mucosal wounds in IBD, current front-line therapies that selectively target mucosal wound healing are not available. Recent studies revealed an association between colonic inflammation and aberrant glycosylation of epithelial CD44v6. Under conditions of inflammation, epithelial CD44v6 was shown to be decorated with the terminal glycan sialyl Lewis A. Importantly, targeting sialylated Lewis glycans on CD44v6 with a murine antibody GM35 was shown to promote mucosal wound healing in cell lines and in biopsy based wounding assays as well as dextran sodium sulfate (DSS) induced murine colitis models. We sequenced CDRs from GM35 and produced a humanized antibody. Eight candidate human IgG1 clones were produced and screened. hPTM-001.4772 was selected from the eight candidates based on glycan affinity and selectivity compared to GM35. In vitro wound healing studies revealed that PTM-001.4772 was as effective as GM35 in promoting repair of scratch wounds with human intestinal epithelial cells. Furthermore, intraperitoneal injection of mice with hPTM-001.4772 during induction of DSS colitis resulted in reduced weight loss compared to control IgG. These results suggest that hPTM-001.4772 is well-positioned as a unique potential candidate therapeutic for IBD that can be used to selectively promote healing of mucosal wounds and ulcers.

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Rigoni, Alice, Richard Poulsom, Rosemary Jeffery, Shameer Mehta, Amy Lewis, Christopher Yau, Eleni Giannoulatou, et al. "Separation of Dual Oxidase 2 and Lactoperoxidase Expression in Intestinal Crypts and Species Differences May Limit Hydrogen Peroxide Scavenging During Mucosal Healing in Mice and Humans." Inflammatory Bowel Diseases 24, no. 1 (December 19, 2017): 136–48. http://dx.doi.org/10.1093/ibd/izx024.

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Abstract Background DUOX2 and DUOXA2 form the predominant H2O2-producing system in human colorectal mucosa. Inflammation, hypoxia, and 5-aminosalicylic acid increase H2O2 production, supporting innate defense and mucosal healing. Thiocyanate reacts with H2O2 in the presence of lactoperoxidase (LPO) to form hypothiocyanate (OSCN-), which acts as a biocide and H2O2 scavenging system to reduce damage during inflammation. We aimed to discover the organization of Duox2, Duoxa2, and Lpo expression in colonic crypts of Lieberkühn (intestinal glands) of mice and how distributions respond to dextran sodium sulfate (DSS)-induced colitis and subsequent mucosal regeneration. Methods We studied tissue from DSS-exposed mice and human biopsies using in situ hybridization, reverse transcription quantitative polymerase chain reaction, and cDNA microarray analysis. Results Duox2 mRNA expression was mostly in the upper crypt quintile while Duoxa2 was more apically focused. Most Lpo mRNA was in the basal quintile, where stem cells reside. Duox2 and Duoxa2 mRNA were increased during the induction and resolution of DSS colitis, while Lpo expression did not increase during the acute phase. Patterns of Lpo expression differed from Duox2 in normal, inflamed, and regenerative mouse crypts (P < 0.001). We found no evidence of LPO expression in the human gut. Conclusions The spatial and temporal separation of H2O2-consuming and -producing enzymes enables a thiocyanate- H2O2 “scavenging” system in murine intestinal crypts to protect the stem/proliferative zones from DNA damage, while still supporting higher H2O2 concentrations apically to aid mucosal healing. The absence of LPO expression in the human gut suggests an alternative mechanism or less protection from DNA damage during H2O2-driven mucosal healing.

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12

Neurath, Markus F. "Mucosal Immunity in Crohn's Disease." Inflammatory Bowel Diseases 10 (February 2004): S29—S31. http://dx.doi.org/10.1097/00054725-200402001-00006.

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Ye, Xiaolin, Jie Wu, Jing Li, and Hongyu Wang. "Anterior Gradient Protein 2 Promotes Mucosal Repair in Pediatric Ulcerative Colitis." BioMed Research International 2021 (May 18, 2021): 1–11. http://dx.doi.org/10.1155/2021/6483860.

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Mucosal healing comprises a key goal of ulcerative colitis (UC) treatment. Anterior gradient protein 2 (AGR2) plays an important role in maintaining intestinal homeostasis in UC. However, the role of AGR2 in the repair of mucosal injury is not yet clear. This study is aimed at investigating the expression of AGR2 in the intestinal tissues of children with UC and its role in repairing mucosal injury. Forty UC patients who were hospitalized in the Pediatric Gastroenterology Ward of Shengjing Hospital affiliated with China Medical University between July 1, 2013, and May 31, 2020, and 20 children who had normal colonoscopy results during the same period (control group) made up the study sample. The disease activity of UC was evaluated based on the pediatric ulcerative colitis activity index, and the ulcerative colitis endoscopic index was evaluated according to the Rachmilewitz score. Immunohistochemical staining was employed to examine the differences in AGR2 expression in the intestinal mucosa between groups. The protective effect of AGR2 in a model of tumor necrosis factor-alpha- (TNF-α-) induced intestinal mucosal barrier injury and the underlying molecular mechanism were explored through in vitro experiments. The results showed that compared with the normal control group, UC patients in the remission or active period had significantly higher expression of AGR2 in the intestine. AGR2 expression was positively correlated with Ki67, an intestinal epithelial cell proliferation marker, but negatively correlated with the degree of endoscopic mucosal injury. In an in vitro model, AGR2 overexpression promoted cell proliferation and migration and inhibited TNF-α-induced intestinal epithelial barrier damage by activating yes-associated protein (YAP). Collectively, our study suggests that AGR2 might serve as a valuable biomarker to help assess the condition and mucosal healing status of UC patients. In vitro, AGR2 promoted the repair of intestinal mucosal barrier injury by activating YAP.

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Lan, Annaïg, François Blachier, Robert Benamouzig, Martin Beaumont, Christophe Barrat, Desire Coelho, Antonio Lancha, et al. "Mucosal Healing in Inflammatory Bowel Diseases." Inflammatory Bowel Diseases 21, no. 1 (January 2015): 198–207. http://dx.doi.org/10.1097/mib.0000000000000177.

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DʼHaens, Geert. "Mucosal Healing in Pediatric Crohnʼs Disease." Inflammatory Bowel Diseases 10, no. 4 (July 2004): 479–80. http://dx.doi.org/10.1097/00054725-200407000-00024.

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Escher, Johanna C. "Mucosal Healing in Pediatric Crohnʼs Disease." Inflammatory Bowel Diseases 10, no. 4 (July 2004): 484. http://dx.doi.org/10.1097/00054725-200407000-00026.

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Diab, Joseph, Terkel Hansen, Rasmus Goll, Hans Stenlund, Maria Ahnlund, Einar Jensen, Thomas Moritz, Jon Florholmen, and Guro Forsdahl. "Lipidomics in Ulcerative Colitis Reveal Alteration in Mucosal Lipid Composition Associated With the Disease State." Inflammatory Bowel Diseases 25, no. 11 (May 11, 2019): 1780–87. http://dx.doi.org/10.1093/ibd/izz098.

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ABSTRACTBackgroundThe onset of ulcerative colitis (UC) is associated with alterations in lipid metabolism and a disruption of the balance between pro- and anti-inflammatory molecules. Only a few studies describe the mucosal lipid biosignatures during active UC. Moreover, the dynamics of lipid metabolism in the remission state is poorly defined. Therefore, this study aims to characterize mucosal lipid profiles in treatment-naïve UC patients and deep remission UC patients compared with healthy subjects.MethodsTreatment-naïve UC patients (n = 21), UC patients in deep remission (n = 12), and healthy volunteers (n = 14) were recruited. The state of deep remission was defined by histological and immunological remission defined by a normalized TNF-α gene expression. Mucosa biopsies were collected by colonoscopy. Lipid analysis was performed by means of ultra-high performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS-MS). In total, 220 lipids from 11 lipid classes were identified.ResultsThe relative concentration of 122 and 36 lipids was altered in UC treatment-naïve patients and UC remission patients, respectively, compared with healthy controls. The highest number of significant variations was in the phosphatidylcholine (PC), ceramide (Cer), and sphingomyelin (SM) composition. Multivariate analysis revealed discrimination among the study groups based on the lipid profile. Furthermore, changes in phosphatidylethanolamine(38:3), Cer(d18:1/24:0), and Cer(d18:1/24:2) were most distinctive between the groups.ConclusionThis study revealed a discriminant mucosal lipid composition pattern between treatment-naïve UC patients, deep remission UC patients, and healthy controls. We report several distinctive lipids, which might be involved in the inflammatory response in UC, and could reflect the disease state.

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Boland, Karen, Tomer Greener, Boyko Kabakchiev, Joanne Stempak, Jenna Tessolini, Rachelle Li, Joelle Soriano, et al. "Identification of Target Golimumab Levels in Maintenance Therapy of Crohn’s Disease and Ulcerative Colitis Associated With Mucosal Healing." Inflammatory Bowel Diseases 26, no. 5 (September 17, 2019): 766–73. http://dx.doi.org/10.1093/ibd/izz199.

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Abstract Introduction Golimumab is approved as a therapy for ulcerative colitis (UC) patients. Recent data also demonstrate efficacy in Crohn’s disease (CD); however, little is known about target drug levels to achieve endoscopic remission. Methods We performed a retrospective analysis of IBD patients on maintenance golimumab. Median trough levels were compared using Kruskal-Wallis test, and logistic regression was used to construct a probabilistic model to determine sensitivity and specificity of levels predicting mucosal healing. Results Fifty-eight patients on maintenance golimumab were included (n = 39 CD, n = 19 UC/IBD-unclassified [IBDU]). Forty percent (n = 23) were cotreated with an immunomodulator, 95% (n = 55) of patients were anti-TNF experienced, and 15.5% (n = 9) had 3 or more prior biologic therapies. Forty-four percent of patients achieved mucosal healing with endoscopic response in a further 26% of patients. Clinical remission was recorded in 41% of patients, and 82% had clinical response. Patients were treated with doses generally higher than the approved maintenance dose. In CD patients, median golimumab trough levels were higher in patients with mucosal healing (8.8 μg/mL vs 5.08 μg/mL, P = 0.03). After calculation of a receiver operating characteristic (ROC) curve for mucosal healing vs nonresponse, a trough level >8 μg/mL was associated with mucosal healing, with 67% sensitivity, 88% specificity, and a likelihood ratio of 3:4. Conclusion Treatment with golimumab was associated with mucosal healing in 44% of all IBD patients. Higher golimumab levels were associated with mucosal healing in CD. These findings support the need for prospective studies to determine target golimumab levels in IBD, which may impact current clinical practices in relation to selection of maintenance dosing.

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Bozkurt, Hüseyin. "P077 A NEW TREATMENT APPROACH FOR INFLAMMATORY BOWEL DISEASE: INTRACOLONIC BIFIDOBACTERIUM AND XYLOGLUCAN APPLICATION." Inflammatory Bowel Diseases 26, Supplement_1 (January 2020): S35—S36. http://dx.doi.org/10.1093/ibd/zaa010.090.

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Abstract Background Inflammatory bowel disease (IBD) pathogenesis includes the altered gut microbiota, environmental factors, human immune responses and genetic. Reduced bifidobacteria level is associated with IBD. Xyloglucan is a plant based prebiotic oligosaccharide. Bifidobacteria level is increased in the presence of xyloglucan. In this article we aim to share the results of our cases; Ulcerative colitis (UC) patients treated by intracolonic single administration of Bifidobacterium animalis subsp. lactis and Xyloglucan combination. Methods Ten UC patients were evaluated; before and after intracolonic single administration of Bifidobacterium animalis subsp. lactis and Xyloglucan combination with colonoscopic laboratory and clinical examination. Results Age, sex, diagnosis, disease location, previous medications are summarized in Table 1. All the patients had active ulcerative colitis disease before the administration. The Mayo Score was used to assess the severity of UC. 2 cases had extensive colitis and 8 patients had left-sided colitis. After 6 weeks of the administration mucosal healing and resolution of colonic symptoms were seen. These results are summarized in Table 2. Of the 10 cases, 7 were undertaken 5-ASA +Azathiopurine and three were undertaken vedolizumab treatment. Intracolonic single Bifidobacterium animalis subsp. lactis and xyloglucan administration was found effective in the mucosal healing and resolution of colonic symptoms in ulcerative colitis patients. Conclusions Herein we reported the importance of Bifidobacterium and xylooligosaccharide combination in IBD. Colonoscopic single Bifidobacterium animalis subsp. lactis and xyloglucan administration is a new method that has no side effect and easy to apply for treatment of IBD.This application might provide enhancement of non-stimulatory status and higher biodiversity in colonic mucosa so mucosal healing may be improved rapidly. However, it would be necessary to develop diagnostic strategies in order to discriminate which patients would benefit from this strategy.

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Bousvaros, Athos. "Mucosal Healing in Children with Crohnʼs Disease." Inflammatory Bowel Diseases 10, no. 4 (July 2004): 481–83. http://dx.doi.org/10.1097/00054725-200407000-00025.

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Kane, Sunanda, Frances Lu, Asher Kornbluth, Dahlia Awais, and Peter D. R. Higgins. "Controversies in mucosal healing in ulcerative colitis." Inflammatory Bowel Diseases 15, no. 5 (May 2009): 796–800. http://dx.doi.org/10.1002/ibd.20875.

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Bozkurt, Hüseyin. "A NEW BACTERIAL TRANSFER THERAPY FOR IBD: ENDOSCOPIC BIFIDOBACTERIUM AND XYLOGLUCAN ADMINISTRATION." Inflammatory Bowel Diseases 27, Supplement_1 (January 1, 2021): S37—S38. http://dx.doi.org/10.1093/ibd/izaa347.091.

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Abstract Ulcerative colitis (UC) pathogenesis includes the altered gut microbiota, environmental factors, and human immune and genetic predisposition. Recently, its association with reduced bifidobacteria quantity in the microbiota is reported.Xyloglucan, a plant based prebiotic oligosaccharide, causes increase in bifidobacteria quantity. In this article we share the results of our UC cases treated by intracolonic single dose administration of Bifidobacterium animalis subsp. Lactis and xyloglucan combination. Intracolonic single dose administration of 200 billion CFUs of Bifidobacterium animalis subsp. lactis and 4 gr of xyloglucan combination was administrated to ten severe UC patients, who were either unresponsive or had inadequate response to treatment. All patients continued treatment after the procedure. Treatment responses were evaluated by colonoscopic, laboratory and clinical examination after 6 weeks. Intracolonic single dose administration of Bifidobacterium animalis subsp. lactis and xyloglucan was found effective in the mucosal healing and resolution of colonic symptoms in ulcerative colitis patients. Intracolonic administration of Bifidobacterium animalis subsp. lactis and xyloglucan in UC is a new single strain and strain specific prebiotic combination method. It is easy to apply and has no observable side effect. Its effectiveness on mucosal healing could be attributed to the enhancement of non-stimulatory status and biodiversity in colonic mucosa. Nonetheless, it is still necessary to develop diagnostic strategies to determine the patients to whom this method would be the most applicable.

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Kominsky, D., S. Keely, E. Campbell, M. Christopher, M. Scully, C. Collins, B. Bowers, and S. Colgan. "A central role of methylation in mucosal inflammation." Inflammatory Bowel Diseases 17, suppl_1 (January 1, 2011): S23. http://dx.doi.org/10.1093/ibd/17.supplement1.s23a.

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Minderhoud, Itta M., Melvin Samsom, and Bas Oldenburg. "What predicts mucosal inflammation in Crohnʼs disease patients?" Inflammatory Bowel Diseases 13, no. 12 (December 2007): 1567–72. http://dx.doi.org/10.1002/ibd.20233.

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Van Assche, Gert. "Does mucosal healing impact patient outcomes long-term?" Inflammatory Bowel Diseases 14, no. 4 (April 2008): 577–78. http://dx.doi.org/10.1002/ibd.20351.

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Suceveanu, Andra Iulia, Laura Mazilu, A. Suceveanu, S. Paris, F. Voinea, Irinel Parepa, and Doina Catrinoiu. "Small bowel capsule endoscopy, a modern tool for celiac disease diagnosis - case presentation." ARS Medica Tomitana 20, no. 2 (May 1, 2014): 86–90. http://dx.doi.org/10.2478/arsm-2014-0016.

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Abstract Celiac disease is a clinically heterogeneous disease characterized by an inadequate immunological response when patients with specific genetic phenotypes are exposed to gluten. This article presents a case of a young woman diagnosed in Gastroenterology Department of “ St. Andrew Apostle” Emergency Hospital of Constanta with celiac disease after multiple admissions into the hospital for unspecific symptoms such as pallor, fatigue, pirosis, weight loss and 1-2 soft stools/day. The history with period irregularities and infertility without a known cause, a recent unexplained bone fracture, the muscle weakness, neuropsychiatric symptoms characterized by sleep disturbances and irritability correlated with the biological features characterized by moderate feriprive anemia, Ca and Mg decreased level, thyroid autoimmune impairment and gastrointestinal symptoms raised the suspicion of an autoimmune disorder with multiple targets. The videcapsule endoscopy (VCE) revealed the specific pattern of the celiac disease: villous atrophy of jejunum, scalloping, absent folds and cobblestone mucosal pattern. Results were correlated with immunology tests results. The patient was transferred on a gluten free diet and the clinical and VCE controlsrevealed the healing of the jejunum mucosa. The VCE can be the tool for positive diagnosis of an unusual and heterogeneous celiac disease in patients with various symptoms without an apparent cause.

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Whiteoak, Simon R., Andrew Claridge, Clare A. Balendran, Richard J. Harris, Markus Gwiggner, Victor P. Bondanese, Fredrik Erlandsson, Mark Berner Hansen, J. R. Fraser Cummings, and Tilman Sanchez-Elsner. "MicroRNA-31 Targets Thymic Stromal Lymphopoietin in Mucosal Infiltrated CD4+ T Cells: A Role in Achieving Mucosal Healing in Ulcerative Colitis?" Inflammatory Bowel Diseases 24, no. 11 (June 8, 2018): 2377–85. http://dx.doi.org/10.1093/ibd/izy213.

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Danese, Silvio, and Livija Deban. "Does the mucosal microcirculation play a role in IBD?" Inflammatory Bowel Diseases 14 (October 2008): S125—S126. http://dx.doi.org/10.1002/ibd.20716.

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Pereira-Fantini, Prue M., Louise M. Judd, Anastasia Kalantzis, Anthony Peterson, Matthias Ernst, Joan K. Heath, and Andrew S. Giraud. "A33 antigen-deficient mice have defective colonic mucosal repair." Inflammatory Bowel Diseases 16, no. 4 (April 2010): 604–12. http://dx.doi.org/10.1002/ibd.21114.

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Elias, César, Cristina Flores, Laura de Bona, André Vilaverde, and Carlos Francesconi. "P-053 Predicators of Mucosal Healing in Ulcerative Colitis." Inflammatory Bowel Diseases 22 (March 2016): S26. http://dx.doi.org/10.1097/01.mib.0000480156.90659.f5.

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Vasquez, Nadia, Irène Mangin, Patricia Lepage, Philippe Seksik, Jean-Paul Duong, Stéphanie Blum, Eduardo Schiffrin, et al. "Patchy distribution of mucosal lesions in ileal Crohnʼs disease is not linked to differences in the dominant mucosa-associated bacteria." Inflammatory Bowel Diseases 13, no. 6 (June 2007): 684–92. http://dx.doi.org/10.1002/ibd.20084.

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Rampal, Ritika, Nahidul Wari, Amit Kumar Singh, Ujjwalkumar Das, Sawan Bopanna, Vipin Gupta, Baibaswata Nayak, et al. "Retinoic Acid Is Elevated in the Mucosa of Patients With Active Ulcerative Colitis and Displays a Proinflammatory Role by Augmenting IL-17 and IFNγ Production." Inflammatory Bowel Diseases 27, no. 1 (May 29, 2020): 74–83. http://dx.doi.org/10.1093/ibd/izaa121.

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Abstract Background All-trans retinoic acid (RA) plays a crucial role in promoting Foxp3+ Treg generation while reciprocally inhibiting Th1/Th17 generation. Our previous research highlighted that in the face of inflammatory conditions, RA plays a contrary role where it aggravates intestinal inflammation by promoting interferon (IFN) γ and interleukin (IL)-17 differentiation in vitro. Methods In this study we translated our in vitro results into a clinical setting where we estimated mucosal and serum RA levels along with the immunophenotypic profile (IL-17, IFNγ, Foxp3, IL-10) in adaptive (CD4, CD8) and innate-like T cells (mucosal associated invariant T cells and γδ T cells) in patients with ulcerative colitis in remission or with active inflammation. Results This is the first study to estimate RA levels in the human gut and shows that patients with active disease had increased mucosal RA levels as compared with patients in remission (4.0 vs 2.5 ng/mL; P < 0.01) and control patients (3.4 vs 0.8 ng/mL; P < 0.0001). This effect was accompanied by significantly elevated IL-17 and IFNγ in tissue CD4+, CD8+, mucosal associated invariant T+ cells, and γδ + T cells. Moreover, the raised RA levels in patients with active disease showed a positive correlation with proinflammatory cytokines (IL-17, IFNγ) and a negative correlation with IL-10. We also found that RA negatively correlated with IL-9, thereby reinstating our previous finding that RA inhibits Th9 differentiation. Conclusions These data confirm our previous in vitro results that in the presence of inflammation, RA plays a crucial role in maintaining gut inflammation by upregulating proinflammatory markers.

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Sarbagili-Shabat, Chen, Dror Weiner, Joram Wardi, Lee Abramas, Michal Yaakov, and Arie Levine. "MODERATE TO SEVERE ENDOSCOPIC INFLAMMATION IS FREQUENT AFTER ACHIEVING CLINICAL REMISSION IN PEDIATRIC ULCERATIVE COLITIS." Inflammatory Bowel Diseases 27, Supplement_1 (January 1, 2021): S13. http://dx.doi.org/10.1093/ibd/izaa347.031.

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Abstract Background Pediatric ulcerative colitis (UC) is characterized by low sustained remission rates and frequent extension of disease even if clinical remission is obtained with therapy. Moderate to severe endoscopic activity is a risk factor for relapse while evidence regarding early mucosal healing or persistence of inflammation after remission in children is not available. Our aim was to evaluate if persistence of significant inflammation is common and could explain the high relapse rate in pediatric UC. Methods Pediatric UC patients with clinical remission, defined as pediatric UC activity index (PUCAI) scores < 10, were prospectively assessed for mucosal healing by endoscopy 3–5 months after remission was documented. Mayo score was assessed for each segment by a blinded adult gastroenterologist using central reading. Symptomatic patients prior to sigmoidoscopy were excluded Sustained remission was assessed retrospectively at 18 months follow-up. Results Forty-six children were enrolled, 28 children in continuous clinical remission at time of sigmoidoscopy were included in the final analysis. Mayo 0 was present in 12/28 (42.86%), Mayo 1 in 2/28 (7.1%) and Mayo 2–3 in 14/28 (50.0%) endoscopies. Among 23/28 patients with follow-up through 18 months, remission was sustained in 2/11 (18.18%) of patients with Mayo 2 and 3 versus 6/12 (50.0%) with Mayo score 0–1. Conclusion Over 50% of children assessed for mucosal healing 3–5 months after clinical remission is obtained have residual disease activity, primarily moderate to severe inflammation which was associated with lower sustained remission. Early sigmoidoscopy after clinical remission for assessment of mucosal disease should be considered in pediatric UC.

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Nancey, Stéphane, Driffa Moussata, Ivan Graber, Sylvette Claudel, Jean-Christophe Saurin, and Bernard Flourié. "Tumor Necrosis Factor α Reduces Butyrate Oxidation In Vitro in Human Colonic Mucosa: A Link from Inflammatory Process to Mucosal Damage?" Inflammatory Bowel Diseases 11, no. 6 (June 2005): 559–66. http://dx.doi.org/10.1097/01.mib.0000161918.04760.f3.

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Davenport, Michael, Jordan Poles, Jacqueline M. Leung, Martin J. Wolff, Wasif M. Abidi, Thomas Ullman, Lloyd Mayer, Ilseung Cho, and Pʼng Loke. "Metabolic Alterations to the Mucosal Microbiota in Inflammatory Bowel Disease." Inflammatory Bowel Diseases 20, no. 4 (April 2014): 723–31. http://dx.doi.org/10.1097/mib.0000000000000011.

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Arijs, Ingrid, Wiebe Vanhove, Paul Rutgeerts, Frans Schuit, Kristin Verbeke, and Vicky De Preter. "Decreased Mucosal Sulfide Detoxification Capacity in Patients With Crohnʼs Disease." Inflammatory Bowel Diseases 19, no. 5 (April 2013): E70—E72. http://dx.doi.org/10.1097/mib.0b013e31827e790e.

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Mullin, Gerard E., Zev R. Maycon, Lorenz Braun-Elwert, Reneé Cerchia, Stephen P. James, Seymour Katz, Gary S. Weissman, Matthew J. McKinley, and Stanley E. Fisher. "Inflammatory Bowel Disease Mucosal Biopsies Have Specialized Lymphokine mRNA Profiles." Inflammatory Bowel Diseases 2, no. 1 (1996): 16–26. http://dx.doi.org/10.1097/00054725-199603000-00004.

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Papadakis, Konstantinos A., and Stephan R. Targan. "The Role of Chemokines and Chemokine Receptors in Mucosal Inflammation." Inflammatory Bowel Diseases 6, no. 4 (November 2000): 303–13. http://dx.doi.org/10.1097/00054725-200011000-00007.

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Reinecker, Hans-Christian. "Dentritic Cell Subspecifications in Mucosal Innate and Adaptive Immune Defenses." Inflammatory Bowel Diseases 12 (April 2006): S4. http://dx.doi.org/10.1097/00054725-200604002-00012.

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Mullin, Gerard E., Zev R. Maycon, Lorenz Braun-Elwert, Reneé Cerchia, Stephen P. James, Seymour Katz, Gary S. Weissman, Matthew J. McKinley, and Stanley E. Fisher. "Inflammatory bowel disease mucosal biopsies have specialized lymphokine mRNA profiles." Inflammatory Bowel Diseases 2, no. 1 (1996): 16–26. http://dx.doi.org/10.1002/ibd.3780020105.

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Papadakis, Konstantinos A., and Stephan R. Targan. "The role of chemokines and chemokine receptors in mucosal inflammation." Inflammatory Bowel Diseases 6, no. 4 (November 2000): 303–13. http://dx.doi.org/10.1002/ibd.3780060408.

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Caldera, Freddy, Dana Ley, Mary S. Hayney, and Francis A. Farraye. "Optimizing Immunization Strategies in Patients with IBD." Inflammatory Bowel Diseases 27, no. 1 (March 31, 2020): 123–33. http://dx.doi.org/10.1093/ibd/izaa055.

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Abstract Recent advances in the treatment of inflammatory bowel disease (IBD) include the use of immune modifiers and monoclonal antibodies, such as tumor necrosis factor (TNF) alpha inhibitors, anti-integrin agents, janus kinase inhibitors, and interleukin-12/23 inhibitors. These agents achieve higher rates of clinical remission and mucosal healing than conventional therapy. However, these therapies increase the risk of infections, including some vaccine-preventable diseases. Infections are one of the most common adverse event of immunosuppressive therapy. Thus, providers should optimize immunization strategies to reduce the risk of vaccine-preventable infections in patients with IBD. There are several newly licensed vaccines recommended for adults by the US Advisory Committee on Immunization Practices. This review will focus on how gastroenterology providers can implement the adult immunization schedule approved by ACIP for patients with IBD.

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Burgueño, Juan F., Adrian Reich, Hajar Hazime, Maria A. Quintero, Irina Fernandez, Julia Fritsch, Ana M. Santander, et al. "Expression of SARS-CoV-2 Entry Molecules ACE2 and TMPRSS2 in the Gut of Patients With IBD." Inflammatory Bowel Diseases 26, no. 6 (April 25, 2020): 797–808. http://dx.doi.org/10.1093/ibd/izaa085.

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Abstract Background Patients with inflammatory bowel disease (IBD) have intestinal inflammation and are treated with immune-modulating medications. In the face of the coronavirus disease-19 pandemic, we do not know whether patients with IBD will be more susceptible to infection or disease. We hypothesized that the viral entry molecules angiotensin I converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) are expressed in the intestine. We further hypothesized that their expression could be affected by inflammation or medication usage. Methods We examined the expression of Ace2 and Tmprss2 by quantitative polymerase chain reacion in animal models of IBD. Publicly available data from organoids and mucosal biopsies from patients with IBD were examined for expression of ACE2 and TMPRSS2. We conducted RNA sequencing for CD11b-enriched cells and peripheral and lamina propria T-cells from well-annotated patient samples. Results ACE2 and TMPRSS2 were abundantly expressed in the ileum and colon and had high expression in intestinal epithelial cells. In animal models, inflammation led to downregulation of epithelial Ace2. Expression of ACE2 and TMPRSS2 was not increased in samples from patients with compared with those of control patients. In CD11b-enriched cells but not T-cells, the level of expression of ACE2 and TMPRSS2 in the mucosa was comparable to other functional mucosal genes and was not affected by inflammation. Anti-tumor necrosis factor drugs, vedolizumab, ustekinumab, and steroids were linked to significantly lower expression of ACE2 in CD11b-enriched cells. Conclusions The viral entry molecules ACE2 and TMPRSS2 are expressed in the ileum and colon. Patients with IBD do not have higher expression during inflammation; medical therapy is associated with lower levels of ACE2. These data provide reassurance for patients with IBD.

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Bandyopadhyay, Chirosree, Leslayann Schecterson, and Barry Gumbiner. "P150 ENHANCING EPITHELIAL BARRIER FUNCTION WITH NOVEL E-CADHERIN ACTIVATING MONOCLONAL ANTIBODIES REDUCES INFLAMMATORY BOWEL DISEASE PROGRESSION IN MOUSE MODELS." Inflammatory Bowel Diseases 26, Supplement_1 (January 2020): S29—S30. http://dx.doi.org/10.1093/ibd/zaa010.071.

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Abstract Deficits in gastrointestinal (GI) epithelial barrier function play important roles in the pathogenesis of Inflammatory Bowel Disease (IBD). The CDH1 gene encoding E-cadherin, a key component of the epithelial junctional complex, is associated with Ulcerative Colitis (UC), and perhaps Crohn’s disease (CD). E-cadherin is the principle adhesive component of the adherens junction, and it regulates paracellular permeability by facilitating the formation of tight junctions and organizing the entire epithelial junction complex. We have identified monoclonal antibodies (mAbs) that bind to E-cadherin and activate adhesion in a variety of epithelial cells. In this study, we aim to test the hypothesis that strengthening E-cadherin adhesion with activating mAbs will enhance barrier function and decrease progression of IBD while maintaining mucosal health and homeostasis. Mouse mAbs to E-cadherin have been tested in vivo using the IL10-knock out mouse and adoptive T cell transfer model of colitis with similar histological evaluation. Transfer of CD4+CD45Rb high T cells from donor to immunocompromised mice produced typical histologic lesions for the adoptive transfer model including inflammation of the mucosa/submucosa, crypt damage, erosions, edema, and epithelial hyperplasia. E-Cadherin activating mAb (r56.4) treatment reduced total colitis score, mucosal hyperplasia, inflammation, gland loss scores, and neutrophilic infiltration in CD45Rb high T cell recipient mice compared to control E-cad mAb (r19.1–10) treatment. In IL10 KO BL6 mouse model of colitis, average lesion severity scores were lower in the r56.4 treatment group in comparison to the r19.1–10 treatment group for all the histological hallmarks of colitis. Further studies are in progress to investigate the therapeutic potential of E-Cadherin mAbs in the rescue of inflammation in pre-clinical mouse models of colitis.

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Stronati, Laura, Anna Negroni, Paola Merola, Veronica Pannone, Osvaldo Borrelli, Manuela Cirulli, Vito Annese, and Salvatore Cucchiara. "Mucosal NOD2 expression and NF-κB activation in pediatric Crohnʼs disease." Inflammatory Bowel Diseases 14, no. 3 (March 2008): 295–302. http://dx.doi.org/10.1002/ibd.20332.

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Han, Seung-Woo, Jeong Min Kim, Yunmee Lho, Hyun Jung Cho, Youn-Kwan Jung, Jung-Ae Kim, Hoyul Lee, Yu-Jeong Lee, and Eun Soo Kim. "DICAM Attenuates Experimental Colitis via Stabilizing Junctional Complex in Mucosal Barrier." Inflammatory Bowel Diseases 25, no. 5 (December 9, 2018): 853–61. http://dx.doi.org/10.1093/ibd/izy373.

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Skupsky, Jonathan, Subrata Sabui, Manando Nakasaki, Michael Hwang, Jana Chen, Michael Cahalan, and Hamid Said. "P130 BIOTIN SUPPLEMENTATION AMELIORATES MURINE COLITIS BY MAINTAINING INTESTINAL MUCOSAL INTEGRITY." Inflammatory Bowel Diseases 25, Supplement_1 (February 2019): S62—S63. http://dx.doi.org/10.1093/ibd/izy393.148.

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Basic, Marijana, Lydia M. Keubler, Manuela Buettner, Marcel Achard, Gerhard Breves, Bernd Schröder, Anna Smoczek, et al. "Norovirus Triggered Microbiota-driven Mucosal Inflammation in Interleukin 10-deficient Mice." Inflammatory Bowel Diseases 20, no. 3 (March 2014): 431–43. http://dx.doi.org/10.1097/01.mib.0000441346.86827.ed.

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Fernandes, Samuel Raimundo, Sónia Bernardo, Carolina Simões, Ana Rita Gonçalves, Ana Valente, Cilénia Baldaia, Paula Moura Santos, Luís Araújo Correia, and Rui Tato Marinho. "Proactive Infliximab Drug Monitoring Is Superior to Conventional Management in Inflammatory Bowel Disease." Inflammatory Bowel Diseases 26, no. 2 (June 27, 2019): 263–70. http://dx.doi.org/10.1093/ibd/izz131.

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In patients with inflammatory bowel disease, proactive therapeutic drug monitoring of infliximab over a 2-year period was associated with higher rates of mucosal healing and lower surgical requirements compared with a conventional cohort treated without therapeutic drug monitoring.

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Kuo, Wei-Ting, Li Zuo, and Jerrold Turner. "THE TIGHT JUNCTION PROTEIN ZO-1 REGULATES MITOTIC SPINDLE ORIENTATION TO ENABLE EFFICIENT MUCOSAL REPAIR." Inflammatory Bowel Diseases 27, Supplement_1 (January 1, 2021): S28. http://dx.doi.org/10.1093/ibd/izaa347.064.

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Abstract The intestinal damage can be caused by physical, infectious, and immune-mediated injury. Rapid repair, which is essential for a return to mucosal homeostasis, depends on rapid epithelial migration, i.e., restitution, as well as epithelial proliferation and differentiation. Barrier restoration is a critical component of this repair process, but the contributions of structural proteins that form the barrier to mucosal repair have not been defined. Aim: To determine the contributions of the intestinal epithelial tight junction protein zonula occludens-1 (ZO-1) to mucosal repair. Results: Intestinal epithelial ZO-1 transcript and protein expression are reduced in biopsies from inflammatory bowel disease (IBD) patients relative to healthy controls. To determine if this ZO-1 loss contributes to disease pathogenesis, we created intestinal epithelial ZO-1-deficient Tjp1f/f x villin-Cre+ mice. When stressed, for example, with 2% DSS, ZO-1-deficient mice displayed much greater mucosal damage and weight loss relative to ZO-1-sufficient mice and failed to recover fully, even 4 weeks after DSS discontinuation. To better define the defect, mice were injected with nucleoside analogs (BrdU and EdU) to label proliferating cells 1 and 3 days after DSS discontinuation. When assessed 2 hours after labeling, numbers of labeled nuclei were significantly reduced in ZO-1-deficient mice relative to ZO-1-sufficient mice. More striking, however, was the nuclear fragmentation and staining for cleaved caspase-3 at 24 hours after labeling. In vitro studies of colonoids were used to better define the mechanisms of epithelial loss. Colonoids from ZO-1-deficient mice were smaller, had reduced numbers of buds (crypt domains) and Lgr5+ stem cells, and were nonresponsive to enhanced Wnt signaling induced by the GSK3 inhibitor CHIR99021, relative to ZO-1-sufficient colonoids. Live imaging of mitosis showed misoriented mitotic spindles in ZO-1-deficient colonoids that caused one daughter cell to lose contact with the extracellular matrix. Misoriented mitotic spindles were also present in tissues from DSS-treated ZO-1-deficient, not ZO-1-sufficient, mice. Live imaging of colonoids from mRFP1-ZO-1 transgenic mice detected transient accumulation of ZO-1 at the cleavage furrow, suggesting that ZO-1 interactions at this site required for accurate mitotic spindle orientation. Conclusion: ZO-1 has a previously unappreciated, noncanonical function in mitotic spindle orientation that is independent of barrier maintenance but central to epithelial proliferation and repair. We postulate that, in the absence of ZO-1, loss of contact with the basement membrane leads to anoikis, i.e., detachment-induced apoptosis, and an abortive proliferative response that compromises repair. We speculate that ZO-1 downregulation in IBD may similarly interfere with mucosal healing. Support: NIH (DK068271, DK061931)

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