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2. Harnessing Digital Pathology And Causal Learning To Improve Eosinophilic Esophagitis Dietary Treatment Assignment

Author

Aknin, Eliel, Larey, Ariel, Caldwell, Julie M., Collins, Margaret H., Abonia, Juan P., Aceves, Seema S., Arva, Nicoleta C., Chehade, Mirna, Dellon, Evan S., Gonsalves, Nirmala, Gupta, Sandeep K., Leung, John, Peterson, Kathryn A., Shoda, Tetsuo, Spergel, Jonathan M., Rothenberg, Marc E., and Savir, Yonatan

Subjects
Computer Science - Machine Learning
Abstract

Eosinophilic esophagitis (EoE) is a chronic, food antigen-driven, allergic inflammatory condition of the esophagus associated with elevated esophageal eosinophils. EoE is a top cause of chronic dysphagia after GERD. Diagnosis of EoE relies on counting eosinophils in histological slides, a manual and time-consuming task that limits the ability to extract complex patient-dependent features. The treatment of EoE includes medication and food elimination. A personalized food elimination plan is crucial for engagement and efficiency, but previous attempts failed to produce significant results. In this work, on the one hand, we utilize AI for inferring histological features from the entire biopsy slide, features that cannot be extracted manually. On the other hand, we develop causal learning models that can process this wealth of data. We applied our approach to the 'Six-Food vs. One-Food Eosinophilic Esophagitis Diet Study', where 112 symptomatic adults aged 18-60 years with active EoE were assigned to either a six-food elimination diet (6FED) or a one-food elimination diet (1FED) for six weeks. Our results show that the average treatment effect (ATE) of the 6FED treatment compared with the 1FED treatment is not significant, that is, neither diet was superior to the other. We examined several causal models and show that the best treatment strategy was obtained using T-learner with two XGBoost modules. While 1FED only and 6FED only provide improvement for 35%-38% of the patients, which is not significantly different from a random treatment assignment, our causal model yields a significantly better improvement rate of 58.4%. This study illustrates the significance of AI in enhancing treatment planning by analyzing molecular features' distribution in histological slides through causal learning. Our approach can be harnessed for other conditions that rely on histology for diagnosis and treatment., Comment: 11 pages, 5 figures

Published
2023

3. Losartan Treatment Reduces Esophageal Eosinophilic Inflammation in a Subset of Eosinophilic Esophagitis

Author

Wechsler, Joshua, Davis, Carla, Furuta, Glenn, Khoury, Paneez, Gupta, Sandeep K., Spergel, Jonathan, Leung, John, Menard-Katcher, Paul, Falk, Gary, Gonsalves, Nirmala Prabu, Peterson, Kathryn, Abonia, J. Pablo, Rudman Spergel, Amanda K., Hirano, Ikuo, Shoda, Tetsuo, Zhang, Xue, Martin, Lisa J., Mukkada, Vincent A., Putnam, Philip E., Blacklidge, Melodie, Neilson, Derek, Collins, Margaret H., Yang, Guang-Yu, Capocelli, Kelley E., Foote, Heather, Eby, Mike, Dong, Stephanie, Aceves, Seema S., and Rothenberg, Marc E.

Published
2024
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4. Clinical and molecular correlates of the Index of Severity for Eosinophilic Esophagitis

Author

Sato, Hiroki, Dellon, Evan S., Aceves, Seema S., Arva, Nicoleta C., Chehade, Mirna, Collins, Margaret H., Davis, Carla M., Falk, Gary W., Furuta, Glenn T., Gonsalves, Nirmala P., Gupta, Sandeep K., Hirano, Ikuo, Hiremath, Girish, Katzka, David A., Khoury, Paneez, Leung, John, Menard-Katcher, Paul, Pesek, Robbie, Peterson, Kathryn A., Pletneva, Maria A., Spergel, Jonathan M., Wechsler, Joshua B., Yang, Guang-Yu, Rothenberg, Marc E., and Shoda, Tetsuo

Published
2024
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8. One-food versus 4-food elimination diet for pediatric eosinophilic esophagitis: A multisite randomized trial

Author

Kliewer, Kara L., Abonia, J. Pablo, Aceves, Seema S., Atkins, Dan, Bonis, Peter A., Capocelli, Kelley E., Chehade, Mirna, Collins, Margaret H., Dellon, Evan S., Fei, Lin, Furuta, Glenn T., Gupta, Sandeep K., Kagalwalla, Amir, Leung, John, Mir, Sabina, Mukkada, Vincent A., Pesek, Robbie, Rosenberg, Chen, Shoda, Tetsuo, Spergel, Jonathan M., Sun, Qin, Wechsler, Joshua B., Yang, Guang-Yu, and Rothenberg, Marc E.

Published
2024
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9. Nonepithelial Gene Expression Correlates With Symptom Severity in Adults With Eosinophilic Esophagitis

Author

Kim, Seung, Ben-Baruch Morgenstern, Netali, Osonoi, Kasumi, Aceves, Seema S., Arva, Nicoleta C., Chehade, Mirna, Collins, Margaret H., Dellon, Evan S., Falk, Gary W., Furuta, Glenn T., Gonsalves, Nirmala P., Gupta, Sandeep K., Hirano, Ikuo, Hiremath, Girish, Katzka, David A., Khoury, Paneez, Leung, John, Pesek, Robbie, Peterson, Kathryn A., Pletneva, Maria A., Spergel, Jonathan M., Wechsler, Joshua B., Yang, Guang-Yu, Rothenberg, Marc E., and Shoda, Tetsuo

Published
2024
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11. Type 2 Immunity and Age Modify Gene Expression of Coronavirus-induced Disease 2019 Receptors in Eosinophilic Gastrointestinal Disorders.

Author

Chiang, Austin, Duong, Loan, Shoda, Tetsuo, Nhu, Quan, Ruffner, Melanie, Hara, Takeo, Aaron, Bailey, Joplin, Erik, Manresa, Mario, Abonia, J, Dellon, Evan, Hirano, Ikuo, Gonsalves, Nirmala, Gupta, Sandeep, Furuta, Glenn, Rothenberg, Marc, Lewis, Nathan, Muir, Amanda, and Aceves, Seema

Subjects
Adult, COVID-19, Child, Enteritis, Eosinophilia, Gastritis, Gene Expression, Humans, Peptidyl-Dipeptidase A, SARS-CoV-2
Abstract

Infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can lead to coronavirus-induced disease 2019 (COVID-19). The gastrointestinal (GI) tract is now an appreciated portal of infection. SARS-CoV-2 enters host cells via angiotensin-converting enzyme-2 (ACE2) and the serine protease TMPRSS2. Eosinophilic gastrointestinal disorders (EGIDs) are inflammatory conditions caused by chronic type 2 (T2) inflammation. the effects of the T2 atopic inflammatory milieu on SARS-COV-2 viral entry gene expression in the GI tract is poorly understood. We analyzed tissue ACE2 and TMPRSS2 gene expression in pediatric eosinophilic esophagitis (EoE), eosinophilic gastritis (EG), and in normal adult esophagi using publicly available RNA-sequencing datasets. Similar to findings evaluating the airway, there was no difference in tissue ACE2/TMPRSS2 expression in EoE or EG when compared with control non-EoE/EG esophagus/stomach. ACE2 gene expression was significantly lower in esophagi from children with or without EoE and from adults with EoE as compared with normal adult esophagi. Type 2 immunity and pediatric age could be protective for infection by SARS-CoV-2 in the gastrointestinal tract because of decreased expression of ACE2.

Published
2021

12. Benralizumab for eosinophilic gastritis: a single-site, randomised, double-blind, placebo-controlled, phase 2 trial

Author

Kliewer, Kara L, Murray-Petzold, Cristin, Collins, Margaret H, Abonia, Juan P, Bolton, Scott M, DiTommaso, Lauren A, Martin, Lisa J, Zhang, Xue, Mukkada, Vincent A, Putnam, Philip E, Kellner, Erinn S, Devonshire, Ashley L, Schwartz, Justin T, Kunnathur, Vidhya A, Rosenberg, Chen E, Lyles, John L, Shoda, Tetsuo, Klion, Amy D, and Rothenberg, Marc E

Published
2023
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14. Local type 2 immunity in eosinophilic gastritis

Author

Ben-Baruch Morgenstern, Netali, Shoda, Tetsuo, Rochman, Yrina, Caldwell, Julie M., Collins, Margaret H., Mukkada, Vincent, Putnam, Philip E., Bolton, Scott M., Felton, Jennifer M., Rochman, Mark, Murray-Petzold, Cristin, Kliewer, Kara L., and Rothenberg, Marc E.

Published
2023
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15. Molecular, endoscopic, histologic, and circulating biomarker-based diagnosis of eosinophilic gastritis: Multi-site study

Author

Shoda, Tetsuo, Wen, Ting, Caldwell, Julie M, Collins, Margaret H, Besse, John A, Osswald, Garrett A, Abonia, J Pablo, Arva, Nicoleta C, Atkins, Dan, Capocelli, Kelley E, Dellon, Evan S, Falk, Gary W, Gonsalves, Nirmala, Gupta, Sandeep K, Hirano, Ikuo, Mukkada, Vincent A, Putnam, Philip E, Sheridan, Rachel M, Spergel, Amanda K Rudman, Spergel, Jonathan M, Wechsler, Joshua B, Yang, Guang-Yu, Aceves, Seema S, Furuta, Glenn T, Rothenberg, Marc E, and Researchers, Consortium of Eosinophilic Gastrointestinal Disease

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Digestive Diseases, Clinical Research, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, Adolescent, Adult, Biomarkers, Child, Cytokines, Endoscopy, Gastrointestinal, Enteritis, Eosinophilia, Female, Gastritis, Humans, Male, Biomarker, diagnostic panel, eosinophil, eosinophilic gastritis, transcriptome, Consortium of Eosinophilic Gastrointestinal Disease Researchers, Immunology, Allergy
Abstract

BackgroundEosinophilic gastritis (EG) is a clinicopathologic disorder with marked gastric eosinophilia and clinical symptoms. There is an unmet need among patients with EG for more precise diagnostic tools.ObjectiveWe aimed to develop tissue- and blood-based diagnostic platforms for EG.MethodsPatients with EG and control subjects without EG were enrolled across 9 Consortium of Eosinophilic Gastrointestinal Disease Researchers-associated sites. An EG Diagnostic Panel (EGDP; gastric transcript subset) and EG blood biomarker panel (protein multiplex array) were analyzed. EGDP18 scores were derived from the expression of 18 highly dysregulated genes, and blood EG scores were derived from dysregulated cytokine/chemokine levels.ResultsGastric biopsy specimens and blood samples from 185 subjects (patients with EG, n = 74; control subjects without EG, n = 111) were analyzed. The EGDP (1) identified patients with active EG (P < .0001, area under the curve ≥ 0.95), (2) effectively monitored disease activity in longitudinal samples (P = .0078), (3) highly correlated in same-patient samples (antrum vs body, r = 0.85, P < .0001), and (4) inversely correlated with gastric peak eosinophil levels (r = -0.83, P < .0001), periglandular circumferential collars (r = -0.73, P < .0001), and endoscopic nodularity (r = -0.45, P < .0001). For blood-based platforms, eotaxin-3, thymus and activation-regulated chemokine, IL-5, and thymic stromal lymphopoietin levels were significantly increased. Blood EG scores (1) distinguished patients with EG from control subjects without EG (P < .0001, area under the curve ≥ 0.91), (2) correlated with gastric eosinophil levels (plasma: r = 0.72, P = .0002; serum: r = 0.54, P = .0015), and (3) inversely correlated with EGDP18 scores (plasma: r = -0.64, P = .0015; serum: r = -0.46, P = .0084). Plasma eotaxin-3 levels strongly associated with gastric CCL26 expression (r = 0.81, P < .0001).ConclusionWe developed tissue- and blood-based platforms for assessment of EG and uncovered robust associations between specific gastric molecular profiles and histologic and endoscopic features, providing insight and clinical readiness tools for this emerging rare disease.

Published
2020

16. One-food versus six-food elimination diet therapy for the treatment of eosinophilic oesophagitis: a multicentre, randomised, open-label trial

Author

Kliewer, Kara L, Gonsalves, Nirmala, Dellon, Evan S, Katzka, David A, Abonia, Juan P, Aceves, Seema S, Arva, Nicoleta C, Besse, John A, Bonis, Peter A, Caldwell, Julie M, Capocelli, Kelley E, Chehade, Mirna, Cianferoni, Antonella, Collins, Margaret H, Falk, Gary W, Gupta, Sandeep K, Hirano, Ikuo, Krischer, Jeffrey P, Leung, John, Martin, Lisa J, Menard-Katcher, Paul, Mukkada, Vincent A, Peterson, Kathryn A, Shoda, Tetsuo, Rudman Spergel, Amanda K, Spergel, Jonathan M, Yang, Guang-Yu, Zhang, Xue, Furuta, Glenn T, and Rothenberg, Marc E

Published
2023
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17. Development and Application of a Functional Human Esophageal Mucosa Explant Platform to Eosinophilic Esophagitis.

Author

Kurten, Richard C, Rawson, Renee, Shoda, Tetsuo, Duong, Loan D, Adejumobi, Dolapo, Levy, Rebecca, Newbury, Robert O, Rothenberg, Marc E, Akuthota, Praveen, Wright, Benjamin L, Dohil, Ranjan, Jones, Stacie M, and Aceves, Seema S

Abstract

There is an increasing prevalence of esophageal diseases but intact human tissue platforms to study esophageal function, disease mechanisms, and the interactions between cell types in situ are lacking. To address this, we utilized full thickness human donor esophagi to create and validate the ex vivo function of mucosa and smooth muscle (n = 25). Explanted tissue was tested for contractile responses to carbachol and histamine. We then treated ex vivo human esophageal mucosa with a cytokine cocktail to closely mimic the Th2 and inflammatory milieu of eosinophilic esophagitis (EoE) and assessed alterations in smooth muscle and extracellular matrix function and stiffening. We found that full thickness human esophagus as well as the individual layers of circular and longitudinal muscularis propria developed tension in response to carbachol ex vivo and that mucosa demonstrated squamous cell differentiation. Treatment of mucosa with Th2 and fibrotic cytokines recapitulated the majority of the clinical Eosinophilic Esophagitis Diagnostic Profile (EDP) on fluidic transcriptional microarray. Transforming growth factor-beta-1 (TGFβ1) increased gene expression of fibronectin, smooth muscle actin, and phospholamban (p

Published
2019

18. Evaluating Eosinophilic Colitis as a Unique Disease Using Colonic Molecular Profiles: A Multi-Site Study

Author

Pablo Abonia, J., Aceves, Seema, Almonte, Samuel, Andrews, Rachel, Anvari, Sara, Arrington, Ashley, Arva, Nicoleta, Atkins, Fred, Bailey, Dominique, Berry, Alexis, Besl, Bridget, Bolton, Scott, Bonis, Peter, Book, Wendy, Bray, Kimberly, Brown, Teresa, Burger, Cassandra, Burke, Deirdre, Cahoon, Jonathon, Capocelli, Kelley, Chehade, Mirna, Chiou, Eric, Collins, Margaret, Davis, Carla, Dellon, Evan, DeMarshall, Maureen, DiTommaso, Lauren, Dohil, Ranjan, Eby, Michael, Falk, Gary, Fleischer, David, Foote, Heather, Foss, Kelci, Friedlander, Joel, Fulkerson, Patricia, Furuta, Glenn, Geno, Debra, Gonsalves, Nirmala, Greuter, Thomas, Gupta, Sandeep, Hamilton, Frank, Harris, Kirk, Harris, Jennifer, Hirano, Ikuo, Hiremath, Girish, Holland-Thomas, Nicole, Jacinto, Lea, Kagalwalla, Amir, Kaseta, Timothy, Katzka, David, Keeley, Kaitlin, Khosh-Hemmat, Emad, Khoury, Paneez, King, Eileen, Kliewer, Kara, Klion, Amy, Knowles, Jennifer, Kocher, Kendra, Kodroff, Ellyn, Krischer, Jeffrey, Kyle, Shay, Leung, John, Levy, Meredith, Liacouras, Chris, Mack, Denise, Martin, Lisa, Martin, Ellen, McCright-Gill, Talaya, Menard-Katcher, Paul, Menard-Katcher, Calies, Mendoza, Gabriela, Mingler, Melissa, Minnicozzi, Mike, Muir, Amanda, Mukkada, Vincent, Murray-Petzold, Cristin, Newbury, Robert, Nhu, Quan, Olive, Anthony, Oyibo, Oghenekpaobor (Joel), Paliana, Allisa, Pan, Zhaoxing, Pesek, Robbie, Peterson, Kathryn, Poppendeck, Heidi, Putnam, Philip, Rivera, Fabian, Rothenberg, Marc, Spergel, Amanda Rudman, Sable, Kathleen, Schoepfer, Alain, Scott, Melissa, Sheridan, Rachel, Sinanovic, Selma, Spergel, Jonathan, Strobel, Mary Jo, Sun, Kiki, Tasco, Amy, Tholen, Crystal, Thompson, Katherine, Tomkinson, Tiffany, Tran, Daisy, Tylicki, Alexandra, Urv, Tiina, Wang, Mei-Lun, Wechsler, Joshua, Wershil, Barry, Wheatley, Lisa, Wilkey, Leah, Yang, Guang-Yu, Zalewski, Angelika, Zicarelli, Amy, Shoda, Tetsuo, Collins, Margaret H., Rochman, Mark, Wen, Ting, Caldwell, Julie M., Mack, Lydia E., Osswald, Garrett A., Besse, John A., Haberman, Yael, Aceves, Seema S., Arva, Nicoleta C., Capocelli, Kelley E., Davis, Carla M., Dellon, Evan S., Falk, Gary W., Gupta, Sandeep K., Mukkada, Vincent A., Putnam, Philip E., Spergel, Jonathan M., Wechsler, Joshua B., Furuta, Glenn T., Denson, Lee A., and Rothenberg, Marc E.

Published
2022
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19. Loss of Endothelial TSPAN12 Promotes Fibrostenotic Eosinophilic Esophagitis via Endothelial Cell–Fibroblast Crosstalk

Author

Abonia, J. Pablo, Aceves, Seema, Almonte, Samuel, Andrews, Rachel, Arrington, Ashley, Arva, Nicoleta, Atkins, Fred, Bailey, Dominique, Berry, Alexis, Besl, Bridget, Bolton, Scott, Bonis, Peter, Book, Wendy, Bray, Kimberly, Brown, Teresa, Burger, Cassandra, Burke, Deirdre, Cahoon, Jonathon, Capocelli, Kelley, Chehade, Mirna, Collins, Margaret, Davis, Carla, Dellon, Evan, DeMarshall, Maureen, DiTommaso, Lauren, Dohil, Ranjan, Eby, Michael, Falk, Gary, Fleischer, David, Foote, Heather, Foss, Kelci, Friedlander, Joel, Fulkerson, Patricia, Furuta, Glenn, Geno, Debra, Gonsalves, Nirmala, Greuter, Thomas, Gupta, Sandeep, Hamilton, Frank, Harris, Kirk, Harris, Jennifer, Hirano, Ikuo, Hiremath, Girish, Holland-Thomas, Nicole, Jacinto, Lea, Kagalwalla, Amir, Kaseta, Timothy, Katzka, David, Keeley, Kaitlin, Khosh-Hemmat, Emad, Khoury, Paneez, King, Eileen, Kliewer, Kara, Klion, Amy, Knowles, Jennifer, Kocher, Kendra, Kodroff, Ellyn, Krischer, Jeffrey, Kyle, Shay, Leung, John, Levy, Meredith, Liacouras, Chris, Mack, Denise, Martin, Lisa, Martin, Ellen, McCright-Gill, Talaya, Menard-Katcher, Paul, Menard-Katcher, Calies, Mendoza, Gabriela, Mingler, Melissa, Minnicozzi, Mike, Muir, Amanda, Mukkada, Vincent, MurrayPetzold, Cristin, Newbury, Robert, Nhu, Quan, Oyibo, Oghenekpaobor (Joel), Paliana, Allisa, Pan, Zhaoxing, Pesek, Robbie, Peterson, Kathryn, Poppendeck, Heidi, Putnam, Philip, Rivera, Fabian, Rothenberg, Marc, Spergel, Amanda Rudman, Sable, Kathleen, Schoepfer, Alain, Scott, Melissa, Sheridan, Rachel, Sinanovic, Selma, Spergel, Jonathan, Strobel, MaryJo, Sun, Kiki, Tasco, Amy, Tholen, Crystal, Thompson, Katherine, Tomkinson, Tiffany, Tran, Daisy, Tylicki, Alexandra, Urv, Tiina, Wang, Mei-Lun, Wechsler, Joshua, Wershil, Barry, Wheatley, Lisa, Wilkey, Leah, Yang, Guang-Yu, Zalewski, Angelika, Zicarelli, Amy, Shoda, Tetsuo, Wen, Ting, Caldwell, Julie M., Ben-Baruch Morgenstern, Netali, Osswald, Garrett A., Rochman, Mark, Mack, Lydia E., Felton, Jennifer M., Arva, Nicoleta C., Atkins, Dan, Bonis, Peter A., Capocelli, Kelley E., Collins, Margaret H., Dellon, Evan S., Falk, Gary W., Gupta, Sandeep K., Menard-Katcher, Paul A., Mukkada, Vincent A., Putnam, Philip E., Rudman Spergel, Amanda K., Spergel, Jonathan M., Wechsler, Joshua B., Aceves, Seema S., Furuta, Glenn T., and Rothenberg, Marc E.

Published
2022
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20. Eosinophilic oesophagitis endotype classification by molecular, clinical, and histopathological analyses: a cross-sectional study.

Author

Abonia, J, Atkins, Dan, Bonis, Peter, Caldwell, Julie, Capocelli, Kelley, Carpenter, Christina, Collins, Margaret, Dellon, Evan, Eby, Michael, Gonsalves, Nirmala, Gupta, Sandeep, Falk, Gary, Hirano, Ikuo, Menard-Katcher, Paul, Kuhl, Jonathan, Krischer, Jeffrey, Leung, John, Mukkada, Vincent, Spergel, Jonathan, Trimarchi, Michael, Yang, Guang-Yu, Zimmermann, Nives, Furuta, Glenn, Rothenberg, Marc, Shoda, Tetsuo, Wen, Ting, and Aceves, Seema

Subjects
Adolescent, Adult, Aged, Biopsy, Child, Child, Preschool, Cross-Sectional Studies, Eosinophilic Esophagitis, Esophagoscopy, Female, Gene Expression Profiling, Humans, Hyperplasia, Leukocyte Count, Machine Learning, Male, Middle Aged, Phenotype, Prospective Studies, Severity of Illness Index, Young Adult
Abstract

BACKGROUND: Eosinophilic oesophagitis is understood in terms of quantifiable histological, endoscopic, and molecular features. Data are scant for inter-relations of these features and their potential to identify distinct disease endotypes. We aimed to identify clinical-pathological correlations between endoscopic and histological disease variables by transcription profiling of the oesophagus of patients with eosinophilic oesophagitis of varying severity and disease activity states. METHODS: We did a cross-sectional study across ten hospital sites in the USA associated with the Consortium of Eosinophilic Gastrointestinal Disease Researchers. We analysed oesophageal biopsy specimens taken from paediatric and adult patients with eosinophilic oesophagitis (discovery cohort), using the eosinophilic oesophagitis diagnostic panel (EDP), a set of 96 informative transcripts. Histological and endoscopic features were assessed by quantification of oesophageal eosinophils and use of the eosinophilic oesophagitis histology scoring system (HSS) and the eosinophilic oesophagitis endoscopic reference score (EREFS). Associations among the various histological, endoscopic, and molecular features were analysed by Spearman correlation. Results were replicated in a biologically independent, single-centre, validation cohort of patients with active eosinophilic oesophagitis. FINDINGS: The discovery cohort contained 185 samples and the validation cohort comprised 100 specimens. In the discovery cohort, EDP showed intersite consistency, significant correlation with oesophageal eosinophils (p

Published
2018

21. Eosinophilic oesophagitis endotype classification by molecular, clinical, and histopathological analyses: a cross-sectional study

Author

Shoda, Tetsuo, Wen, Ting, Aceves, Seema S, Abonia, J Pablo, Atkins, Dan, Bonis, Peter A, Caldwell, Julie M, Capocelli, Kelley E, Carpenter, Christina L, Collins, Margaret H, Dellon, Evan S, Eby, Michael D, Gonsalves, Nirmala, Gupta, Sandeep K, Falk, Gary W, Hirano, Ikuo, Menard-Katcher, Paul, Kuhl, Jonathan T, Krischer, Jeffrey P, Leung, John, Mukkada, Vincent A, Spergel, Jonathan M, Trimarchi, Michael P, Yang, Guang-Yu, Zimmermann, Nives, Furuta, Glenn T, Rothenberg, Marc E, and Researchers, Consortium of Eosinophilic Gastrointestinal Disease

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Aetiology, Adolescent, Adult, Aged, Biopsy, Child, Child, Preschool, Cross-Sectional Studies, Eosinophilic Esophagitis, Esophagoscopy, Female, Gene Expression Profiling, Humans, Hyperplasia, Leukocyte Count, Machine Learning, Male, Middle Aged, Phenotype, Prospective Studies, Severity of Illness Index, Young Adult, Consortium of Eosinophilic Gastrointestinal Disease Researchers, Clinical sciences
Abstract

BackgroundEosinophilic oesophagitis is understood in terms of quantifiable histological, endoscopic, and molecular features. Data are scant for inter-relations of these features and their potential to identify distinct disease endotypes. We aimed to identify clinical-pathological correlations between endoscopic and histological disease variables by transcription profiling of the oesophagus of patients with eosinophilic oesophagitis of varying severity and disease activity states.MethodsWe did a cross-sectional study across ten hospital sites in the USA associated with the Consortium of Eosinophilic Gastrointestinal Disease Researchers. We analysed oesophageal biopsy specimens taken from paediatric and adult patients with eosinophilic oesophagitis (discovery cohort), using the eosinophilic oesophagitis diagnostic panel (EDP), a set of 96 informative transcripts. Histological and endoscopic features were assessed by quantification of oesophageal eosinophils and use of the eosinophilic oesophagitis histology scoring system (HSS) and the eosinophilic oesophagitis endoscopic reference score (EREFS). Associations among the various histological, endoscopic, and molecular features were analysed by Spearman correlation. Results were replicated in a biologically independent, single-centre, validation cohort of patients with active eosinophilic oesophagitis.FindingsThe discovery cohort contained 185 samples and the validation cohort comprised 100 specimens. In the discovery cohort, EDP showed intersite consistency, significant correlation with oesophageal eosinophils (p

Published
2018

24. Effects of Proton Pump Inhibitors on Esophageal Remodeling and Fibrosis in Eosinophilic Esophagitis

Author

Sharlin, Colby, primary, Maekawa, Yuki, additional, Sato, Hiroki, additional, Matsuyama, Kazuhiro, additional, Kim, Seung, additional, Osonoi, Kasumi, additional, Sakai, Naoya, additional, Osswald, Garrett, additional, Rochman, Mark, additional, Wen, Ting, additional, Dellon, Evan, additional, Rothenberg, Marc, additional, and Shoda, Tetsuo, additional

Published
2024
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26. Desmoplakin and periplakin genetically and functionally contribute to eosinophilic esophagitis

Author

Shoda, Tetsuo, Kaufman, Kenneth M., Wen, Ting, Caldwell, Julie M., Osswald, Garrett A., Purnima, Pathre, Zimmermann, Nives, Collins, Margaret H., Rehn, Kira, Foote, Heather, Eby, Michael D., Zhang, Wenying, Ben-Baruch Morgenstern, Netali, Ballaban, Adina Y., Habel, Jeff E., Kottyan, Leah C., Abonia, J. Pablo, Mukkada, Vincent A., Putnam, Philip E., Martin, Lisa J., and Rothenberg, Marc E.

Published
2021
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36. Prospective Endoscopic Activity Assessment for Eosinophilic Gastritis in a Multisite Cohort

Author

Hirano, Ikuo, Collins, Margaret H., King, Eileen, Sun, Qin, Chehade, Mirna, Abonia, J Pablo., Bonis, Peter A., Capocelli, Kelly E., Dellon, Evan S., Falk, Gary W., Gonsalves, Nirmala, Gupta, Sandeep K., Leung, John, Katzka, David, Menard-Katcher, Paul, Khoury, Paneez, Klion, Amy, Mukkada, Vincent A., Peterson, Kathryn, Shoda, Tetsuo, Rudman-Spergel, Amanda K., Spergel, Jonathan A., Yang, Guang-Yu, Rothenberg, Marc E., Aceves, Seema S., and Furuta, Glenn T.

Subjects
Adult, Hepatology, Gastritis, Eosinophilia, Gastroenterology, Humans, Eosinophilic Esophagitis, Child, Article, Endoscopy, Gastrointestinal, Enteritis
Abstract

INTRODUCTION: Eosinophilic gastritis (EG) is a chronic, inflammatory disease of the stomach characterized by eosinophil-predominant, gastric mucosal inflammation and gastrointestinal symptoms. The aim of this study was to prospectively evaluate endoscopic features in a large series of children and adults with EG to better understand the endoscopic manifestations and develop a standardized instrument for investigations. METHODS: Data were prospectively collected as part of the Consortium for Eosinophilic Gastrointestinal Disease Researchers (CEGIR), a national collaborative network. Endoscopic features were prospectively recorded using a system specifically developed for EG, the Eosinophilic Gastritis Endoscopic Reference System (EG-REFS). Correlations were made between EG-REFS and clinical and histologic features. RESULTS: Of 98 patients with EG, 65 underwent assessment using EG-REFS. The most common findings were erythema (72%), raised lesions (49%), erosions (46%) and granularity (35%); only 8% of patients with active histology (≥30 eosinophils/hpf) had no endoscopic findings. A strong correlation between EG-REFS scores and physician global assessment of endoscopy severity was demonstrated (Spearman r = 0.84, P

Published
2022

37. Molecular analysis of duodenal eosinophilia

Author

Shoda, Tetsuo, primary, Rochman, Mark, additional, Collins, Margaret H., additional, Caldwell, Julie M., additional, Mack, Lydia E., additional, Osswald, Garrett A., additional, Mukkada, Vincent A., additional, Putnam, Philip E., additional, and Rothenberg, Marc E., additional

Published
2022
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39. Epithelial cell‐expressed type II IL ‐4 receptor mediates eosinophilic esophagitis

Author

Avlas, Shmulik, primary, Shani, Guy, additional, Rhone, Natalie, additional, Itan, Michal, additional, Dolitzky, Avishay, additional, Hazut, Inbal, additional, Grisaru‐Tal, Sharon, additional, Gordon, Yaara, additional, Shoda, Tetsuo, additional, Ballaban, Adina, additional, Ben‐Baruch, Netali Morgenstern, additional, Rochman, Mark, additional, Diesendruck, Yael, additional, Nahary, Limor, additional, Bitton, Almog, additional, Halpern, Zamir, additional, Benhar, Itai, additional, Varol, Chen, additional, Rothenberg, Marc E., additional, and Munitz, Ariel, additional

Published
2022
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41. Single-cell RNA sequencing of mast cells in eosinophilic esophagitis reveals heterogeneity, local proliferation, and activation that persists in remission

Author

Ben-Baruch Morgenstern, Netali, primary, Ballaban, Adina Y., additional, Wen, Ting, additional, Shoda, Tetsuo, additional, Caldwell, Julie M., additional, Kliewer, Kara, additional, Felton, Jennifer M., additional, Abonia, J. Pablo, additional, Mukkada, Vincent A., additional, Putnam, Philip E., additional, Bolton, Scott M., additional, Dwyer, Daniel F., additional, Barrett, Nora A., additional, and Rothenberg, Marc E., additional

Published
2022
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42. The mast cell pain connection in eosinophilic esophagitis

Author

Zhang, Simin, Shoda, Tetsuo, Aceves, Seema S., Arva, Nicoleta C., Chehade, Mirna, Collins, Margaret H., Dellon, Evan S., Falk, Gary W., Gonsalves, Nirmala, Gupta, Sandeep K., Hirano, Ikuo, Khoury, Paneez, Leung, John, Rudman Spergel, Amanda K., Spergel, Jonathan M., Wechsler, Joshua B., Yang, Guang-Yu, Furuta, Glenn T., and Rothenberg, Marc E.

Subjects
Gastritis, Immunology, Eosinophilia, Immunology and Allergy, Humans, Pain, Eosinophilic Esophagitis, Mast Cells, Article, Enteritis
Published
2022

43. Molecular analysis of duodenal eosinophilia.

Author

Shoda, Tetsuo, Rochman, Mark, Collins, Margaret H., Caldwell, Julie M., Mack, Lydia E., Osswald, Garrett A., Mukkada, Vincent A., Putnam, Philip E., and Rothenberg, Marc E.

Abstract

Eosinophilic duodenitis (EoD), characterized by nonspecific gastrointestinal symptoms and increased numbers of duodenal eosinophils, may be in the eosinophilic gastrointestinal disease spectrum. However, diagnostic thresholds and pathogenic processes of duodenal tissue eosinophilia are inadequately characterized. We aimed to define an EoD transcriptome and pathologic pathways. RNA sequencing and histologic features of human duodenal biopsy samples were analyzed as a function of duodenal eosinophils levels. For analyses, we defined EoD as more than 52 peak eosinophils/hpf (n = 8), duodenal eosinophilia as 30 to 52 eosinophils/hpf (n = 11), and normal controls as fewer than 30 eosinophils/hpf (n = 8). Associations between gene expression and histologic features were analyzed with Spearman correlation. We identified 382 differentially expressed genes (EoD transcriptome) between EoD and normal controls (>2-fold change [adjusted P <.05]). The EoD transcriptome distinguished EoD from controls (duodenal eosinophilia and normal controls). The duodenal eosinophil count was correlated with a distinct EoD transcriptome when 50 to 60 peak eosinophils/hpf were present. The EoD transcriptome was enriched in genes involved in IL-4/IL-13 signaling, mast cells, and myeloid progenitor cells. Among duodenal histologic features, lamina propria eosinophil sheets was the most associated with transcriptomic changes (r = 0.66; P <.01). EoD gene signatures were shared with eosinophilic esophagitis and eosinophilic gastritis but not with eosinophilic colitis or celiac disease. We have identified an EoD transcriptomic signature that emerges at 50 to 60 peak eosinophils/hpf and established EoD as part of a spectrum of upper eosinophilic gastrointestinal disorder associated with type 2 immunity and distinct from eosinophilic colitis and celiac disease. These findings provide a basis for improving diagnosis and treatment. [Display omitted] [ABSTRACT FROM AUTHOR]

Published
2023
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44. Evaluating Eosinophilic Colitis as a Unique Disease Using Colonic Molecular Profiles: A Multi-Site Study

Author

Shoda, Tetsuo, primary, Collins, Margaret H., additional, Rochman, Mark, additional, Wen, Ting, additional, Caldwell, Julie M., additional, Mack, Lydia E., additional, Osswald, Garrett A., additional, Besse, John A., additional, Haberman, Yael, additional, Aceves, Seema S., additional, Arva, Nicoleta C., additional, Capocelli, Kelley E., additional, Chehade, Mirna, additional, Davis, Carla M., additional, Dellon, Evan S., additional, Falk, Gary W., additional, Gonsalves, Nirmala, additional, Gupta, Sandeep K., additional, Hirano, Ikuo, additional, Khoury, Paneez, additional, Klion, Amy, additional, Menard-Katcher, Calies, additional, Leung, John, additional, Mukkada, Vincent A., additional, Putnam, Philip E., additional, Spergel, Jonathan M., additional, Wechsler, Joshua B., additional, Yang, Guang-Yu, additional, Furuta, Glenn T., additional, Denson, Lee A., additional, Rothenberg, Marc E., additional, Pablo Abonia, J., additional, Aceves, Seema, additional, Almonte, Samuel, additional, Andrews, Rachel, additional, Anvari, Sara, additional, Arrington, Ashley, additional, Arva, Nicoleta, additional, Atkins, Fred, additional, Bailey, Dominique, additional, Berry, Alexis, additional, Besl, Bridget, additional, Bolton, Scott, additional, Bonis, Peter, additional, Book, Wendy, additional, Bray, Kimberly, additional, Brown, Teresa, additional, Burger, Cassandra, additional, Burke, Deirdre, additional, Cahoon, Jonathon, additional, Capocelli, Kelley, additional, Chiou, Eric, additional, Collins, Margaret, additional, Davis, Carla, additional, Dellon, Evan, additional, DeMarshall, Maureen, additional, DiTommaso, Lauren, additional, Dohil, Ranjan, additional, Eby, Michael, additional, Falk, Gary, additional, Fleischer, David, additional, Foote, Heather, additional, Foss, Kelci, additional, Friedlander, Joel, additional, Fulkerson, Patricia, additional, Furuta, Glenn, additional, Geno, Debra, additional, Greuter, Thomas, additional, Gupta, Sandeep, additional, Hamilton, Frank, additional, Harris, Kirk, additional, Harris, Jennifer, additional, Hiremath, Girish, additional, Holland-Thomas, Nicole, additional, Jacinto, Lea, additional, Kagalwalla, Amir, additional, Kaseta, Timothy, additional, Katzka, David, additional, Keeley, Kaitlin, additional, Khosh-Hemmat, Emad, additional, King, Eileen, additional, Kliewer, Kara, additional, Knowles, Jennifer, additional, Kocher, Kendra, additional, Kodroff, Ellyn, additional, Krischer, Jeffrey, additional, Kyle, Shay, additional, Levy, Meredith, additional, Liacouras, Chris, additional, Mack, Denise, additional, Martin, Lisa, additional, Martin, Ellen, additional, McCright-Gill, Talaya, additional, Menard-Katcher, Paul, additional, Mendoza, Gabriela, additional, Mingler, Melissa, additional, Minnicozzi, Mike, additional, Muir, Amanda, additional, Mukkada, Vincent, additional, Murray-Petzold, Cristin, additional, Newbury, Robert, additional, Nhu, Quan, additional, Olive, Anthony, additional, Oyibo, Oghenekpaobor (Joel), additional, Paliana, Allisa, additional, Pan, Zhaoxing, additional, Pesek, Robbie, additional, Peterson, Kathryn, additional, Poppendeck, Heidi, additional, Putnam, Philip, additional, Rivera, Fabian, additional, Rothenberg, Marc, additional, Spergel, Amanda Rudman, additional, Sable, Kathleen, additional, Schoepfer, Alain, additional, Scott, Melissa, additional, Sheridan, Rachel, additional, Sinanovic, Selma, additional, Spergel, Jonathan, additional, Strobel, Mary Jo, additional, Sun, Kiki, additional, Tasco, Amy, additional, Tholen, Crystal, additional, Thompson, Katherine, additional, Tomkinson, Tiffany, additional, Tran, Daisy, additional, Tylicki, Alexandra, additional, Urv, Tiina, additional, Wang, Mei-Lun, additional, Wechsler, Joshua, additional, Wershil, Barry, additional, Wheatley, Lisa, additional, Wilkey, Leah, additional, Zalewski, Angelika, additional, and Zicarelli, Amy, additional

Published
2022
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45. Esophageal Mast cells in Eosinophilic Esophagitis Are Heterogeneous, Dynamically Activated and Locally Proliferate

Author

Ben-Baruch Morgenstern, Netali, primary, Ballaban, Adina, additional, Wen, Ting, additional, Shoda, Tetsuo, additional, Caldwell, Julie, additional, Kliewer, Kara, additional, Felton, Jennifer, additional, Abonia, Juan, additional, Mukkada, Vincent, additional, Putnam, Philip, additional, Bolton, Scott, additional, Dwyer, Daniel, additional, Barrett, Nora, additional, and Rothenberg, Marc, additional

Published
2022
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47. Loss of Endothelial TSPAN12 Promotes Fibrostenotic Eosinophilic Esophagitis via Endothelial Cell–Fibroblast Crosstalk

Author

Shoda, Tetsuo, primary, Wen, Ting, additional, Caldwell, Julie M., additional, Ben-Baruch Morgenstern, Netali, additional, Osswald, Garrett A., additional, Rochman, Mark, additional, Mack, Lydia E., additional, Felton, Jennifer M., additional, Abonia, J. Pablo, additional, Arva, Nicoleta C., additional, Atkins, Dan, additional, Bonis, Peter A., additional, Capocelli, Kelley E., additional, Collins, Margaret H., additional, Dellon, Evan S., additional, Falk, Gary W., additional, Gonsalves, Nirmala, additional, Gupta, Sandeep K., additional, Hirano, Ikuo, additional, Leung, John, additional, Menard-Katcher, Paul A., additional, Mukkada, Vincent A., additional, Putnam, Philip E., additional, Rudman Spergel, Amanda K., additional, Spergel, Jonathan M., additional, Wechsler, Joshua B., additional, Yang, Guang-Yu, additional, Aceves, Seema S., additional, Furuta, Glenn T., additional, Rothenberg, Marc E., additional, Aceves, Seema, additional, Almonte, Samuel, additional, Andrews, Rachel, additional, Arrington, Ashley, additional, Arva, Nicoleta, additional, Atkins, Fred, additional, Bailey, Dominique, additional, Berry, Alexis, additional, Besl, Bridget, additional, Bolton, Scott, additional, Bonis, Peter, additional, Book, Wendy, additional, Bray, Kimberly, additional, Brown, Teresa, additional, Burger, Cassandra, additional, Burke, Deirdre, additional, Cahoon, Jonathon, additional, Capocelli, Kelley, additional, Chehade, Mirna, additional, Collins, Margaret, additional, Davis, Carla, additional, Dellon, Evan, additional, DeMarshall, Maureen, additional, DiTommaso, Lauren, additional, Dohil, Ranjan, additional, Eby, Michael, additional, Falk, Gary, additional, Fleischer, David, additional, Foote, Heather, additional, Foss, Kelci, additional, Friedlander, Joel, additional, Fulkerson, Patricia, additional, Furuta, Glenn, additional, Geno, Debra, additional, Greuter, Thomas, additional, Gupta, Sandeep, additional, Hamilton, Frank, additional, Harris, Kirk, additional, Harris, Jennifer, additional, Hiremath, Girish, additional, Holland-Thomas, Nicole, additional, Jacinto, Lea, additional, Kagalwalla, Amir, additional, Kaseta, Timothy, additional, Katzka, David, additional, Keeley, Kaitlin, additional, Khosh-Hemmat, Emad, additional, Khoury, Paneez, additional, King, Eileen, additional, Kliewer, Kara, additional, Klion, Amy, additional, Knowles, Jennifer, additional, Kocher, Kendra, additional, Kodroff, Ellyn, additional, Krischer, Jeffrey, additional, Kyle, Shay, additional, Levy, Meredith, additional, Liacouras, Chris, additional, Mack, Denise, additional, Martin, Lisa, additional, Martin, Ellen, additional, McCright-Gill, Talaya, additional, Menard-Katcher, Paul, additional, Menard-Katcher, Calies, additional, Mendoza, Gabriela, additional, Mingler, Melissa, additional, Minnicozzi, Mike, additional, Muir, Amanda, additional, Mukkada, Vincent, additional, MurrayPetzold, Cristin, additional, Newbury, Robert, additional, Nhu, Quan, additional, Oyibo, Oghenekpaobor (Joel), additional, Paliana, Allisa, additional, Pan, Zhaoxing, additional, Pesek, Robbie, additional, Peterson, Kathryn, additional, Poppendeck, Heidi, additional, Putnam, Philip, additional, Rivera, Fabian, additional, Rothenberg, Marc, additional, Spergel, Amanda Rudman, additional, Sable, Kathleen, additional, Schoepfer, Alain, additional, Scott, Melissa, additional, Sheridan, Rachel, additional, Sinanovic, Selma, additional, Spergel, Jonathan, additional, Strobel, MaryJo, additional, Sun, Kiki, additional, Tasco, Amy, additional, Tholen, Crystal, additional, Thompson, Katherine, additional, Tomkinson, Tiffany, additional, Tran, Daisy, additional, Tylicki, Alexandra, additional, Urv, Tiina, additional, Wang, Mei-Lun, additional, Wechsler, Joshua, additional, Wershil, Barry, additional, Wheatley, Lisa, additional, Wilkey, Leah, additional, Zalewski, Angelika, additional, and Zicarelli, Amy, additional

Published
2022
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49. A connection found between mast cells and pain in eosinophilic esophagitis

Author

Zhang, Simin, primary, Shoda, Tetsuo, additional, Aceves, Seema, additional, Chehade, Mirna, additional, Collins, Margaret, additional, Davis, Carla, additional, Dellon, Evan, additional, Falk, Gary, additional, Furuta, Glenn, additional, Gonsalves, Nirmala, additional, Gupta, Sandeep, additional, Hirano, Ikuo, additional, Khoury, Paneez, additional, Leung, John, additional, Peterson, Kathryn, additional, Spergel, Jonathan, additional, Wechsler, Joshua, additional, Yang, Guang-Yu, additional, and Rothenberg, Marc, additional

Published
2022
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50. Strong association of mast cells with eosinophilic esophagitis‐specific signatures.

Author

Alvarado, Diego, Lu, Yufang, Shoda, Tetsuo, Caldwell, Julie M., Keler, Tibor, and Rothenberg, Marc E.

Subjects
EOSINOPHILIC esophagitis, MAST cells
Abstract

Given the limited clinical effect of eosinophil-directed therapies in EoE to date, our data support exploring the clinical benefit of anti-MC agents in EoE. Pearson correlations performed with MC-specific protease carboxypeptidase A3 ( I CPA3 i ) demonstrated a strong correlation with eosinophil transcriptional signatures, including the eotaxin receptor I CCR3 i , the eosinophil granule lysophospholipase ( I CLC i ), and the eosinophil chemokines eotaxin-3 ( I CCL26 i ) and I IL5 i (Figures 1 and 2A). Abbreviations EoE eosinophilic esophagitis EDP eosinophilic esophagitis diagnostic panel MC mast cell PEC peak eosinophil count Eosinophilic esophagitis (EoE) is a type 2 inflammatory disorder characterized by esophageal inflammation, eosinophil infiltration, tissue remodeling, and stricture.[1] Currently, diagnosis of EoE is based on clinical assessments and a peak tissue eosinophil count (PEC) of >=15 eosinophils per high powered field, although PEC does not correlate well with symptom severity, and eosinophil reduction to normal levels does not correlate with symptomatic improvement in some studies.[1] Numerous studies have demonstrated that mast cells (MCs) are also present in significantly greater numbers in EoE than in normal esophageal biopsies. [Extracted from the article]

Published
2023
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