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1. WAO International Scientific Conference (WISC 2016) Abstracts

Author

Jun Bao, Yi-Hui Wang, Quan-Hua Liu, Yi-Xiao Bao, Nurit Azouz, Julie Caldwell, Leanne Ray, Mark Rochman, Melissa Mingler, Matthew Eilerman, Ting Wen, Jocelyn Biagini Myers, Gurjit Khurana Hershey, Leah Kottyan, Lisa Martin, Rothenberg Marc, Victor Gonzalez-Uribe, Jaime Del Rio-Chivardi, Blanca Del Rio-Navarro, Hongfei Lou, Siyuan Ma, Yan Zhao, Feifei Cao, Fei He, Zhongyan Liu, Chengshuo Wang, Claus Bachert, Luo Zhang, Elissa Abrams, Allan Becker, Amit Kandhare, Subhash Bodhankar, Nicole Grossman, Gheorghe Doros, Francine Laden, Anne Fuhlbrigge, Michael Wechsler, Wilson Pace, Barbara Yawn, Elliot Israel, Junehyuk Lee, Frederick Adler, Peter Kim, Yung Feng Huang, Ying Yao Chen, Chiun Yen Pan, Herng Sheng Lee, Michael Khalemsky, David G. Schwartz, Pavel Kolkhir, Dmitry Pogorelov, Nikolay Kochergin, Hirsh Komarow, Michael Young, Robin Eisch, Linda Scott, Dean Metcalfe, Alexander Singer, Andrew Wakeman, Thomas Gerstner, Woo-Jung Song, Ji-Su Shim, Ha-Kyeong Won, Sung-Yoon Kang, Kyoung-Hee Sohn, Byung-Keun Kim, Eun-Jung Jo, Min-Hye Kim, Sang-Heon Kim, Heung-Woo Park, Sun-Sin Kim, Yoon-Seok Chang, Alyn H. Morice, Byung-Jae Lee, Sang-Heon Cho, Kyung-Up Min, Maria Assunta Boscolo, Giulio Brivio, Sergio Bosisio, Nicoletta Manzocchi, Edoardo Pulixi, Giulia Grignani, Eloisia D’Andrea, Massimo Ricci, Elena Passini, Maurizio Italia, Marilyn Urrutia-Pereira, Stefani Fagundes, Vinicius Jardim Oliano, Dirceu Solé, Sadia Benzaquen, Alejandro Aragaki, Ricardo Balestra, Dawn Harden, Danielle Caudell-Stamper, Gilbert Glady, Mark Holbreich, Nataliya Lyakhovska, Igor Kaidashev, Jaromir Bystron, Beata Hutyrova, Galina Balakirski, Luk Vanstreels, Gerda Wurpts, Hans F. Merk, Jens Malte Baron, Johanna Plange, Hans-Peter Rihs, Monika Raulf, Stefani Roeseler, Alberto Tolcachier, Armando Chamorro, Ruth Otero, Joel Brooks, Michael Hess, Jared Benz, Joseph MacDonald, Usma Chatha, Dale Lent, Şükran Köse, Bengü Gireniz Tatar, Gülgün Akkoçlu, İbrahim Çukurova, İlker Ödemiş, Ayşin Kılınç Toker, Abdullahi Hasssan, Abdulrazaq Abdullahi Gobir, Cheol-Woo Kim, Young Hwa Choi, Jeong Hye Lee, Rae Jeong Cho, Yu Ran Nam, Joo Hyun Nam, Woo Kyung Kim, Ivana Filipovic, Zorica Zivkovic, Djordje Filipovic, Dana Shik, Andrew Smith, Wang Yui Hsi, Stuart Friedman, Yonatan Gizaw, Rima Bakhda, Kumail Mohammed, Richard Wasserman, Angela Hague, Deanna Pence, Joanna Rolen, Robert Sugerman, Stacy Silvers, Qurat Kamili, Nadezhda Knauer, Alexandr Zazernyi, Elena Blinova, Daria Demina, Vladimir Kozlov, Komal Agrawal, Sagar Kale, Naveen Arora, Volha Vasilkova, Tatiana Mokhort, William Silvers, Rachel Eisenberg, Rushita Mehta, Arye Rubinstein, Antony Aston, Paul Turner, Monica Ruiz-Garcia, Robert Boyle, Simon Brown, Yael Dinur Schejter, Adi Ovadia, Vy Kim, Brenda Reid, Chaim Roifman, Lana Rosenfield, Ernie Avilla, Laurie Harada, Marilyn Allen, Susan Waserman, Ho Joo Yoon, Gun Woo Koo, Suk-Il Chang, Hye-Ran Yoon, Dong Won Park, Tai Sun Park, Ji-Yong Moon, Tae Hyung Kim, Jang Won Sohn, Dong Ho Shin, Tsici Jorjoliani, Lia Jorjoliani, Nino Adamia, Nona katamadze, Deepika Ramachandra, Liana Jorjoliani, Rusudan Karseladze, Lali Saginadze, Natalia Chkuaseli, Anna Dolgova, Olga Stukolova, Anna Sudina, Anna Cherkashina, German Shipulin, Richard Rosenthal, Harvey Howe, Paul Knause, Rony Greemberg, Jean Jacques De Bruycker, Isabel Fernandez, Françoise Le Deist, Elie Haddad, Yeong Ho Rha, Kyung Suk Lee, Sun Hee Choi, Herman Tam, Estelle Simons, Elinor Simons, Maria Golebiowska-Wawrzyniak, Katarzyna Markiewicz, Yoram Faitelson, Miguel Stein, Avigdor Mandelberg, Ilan Dalal, Michael Levin, Lelani Hobane, Wisdom Basera, Maresa Botha, Claudia Gray, Heather Zar, Biserka Jovkovska Kjaeva, Zoran Arsovski, Vesna Grivcheva-Panovska, Adeyinka Odebode, Adedotun Adekunle, Peter Adeonipekun, Ebenezer Farombi, Nadezhda Camacho-Ordoñez, Alejandrina Josefina Martinez-Vázquez, María de la Luz H. García-Cruz, Qi Tan, Rui Min, Guan-qun Dai, Wei-Ping Xie, Huang Mao, Hong Wang, Rakesh Yadav, Sneha Singh, Divya Yadav, Ekaterina Khaleva, Henry T. Bahnson, Amber Franz, Lene Heise Garvey, Nicola Jay, Rubaiyat Haque, Adam Fox, Gideon Lack, George du Toit, Snezana Radic, Branislava Milenkovic, Ana Neskovic, Ljiljana Danojevic, Liat Nachshon, Michael Goldberg, Michael Levy, Yitzhak Katz, Arnon Elizur, Cristine Rosario, Juliana Kasper, Herbeto Chong-Neto, Carlos Riedi, Nelson Rosario, Michael B. Levy, Ronly Har-Even, Mor Carmel, Michael R. Goldberg, Maia Kherkheulidze, Nani Kavlashvili, Eka Kandelaki, Nino Adamai, Irma Ubiria, Andrea Burke, Monika Kastner, Denica Zheleva, Razvigor Darlenski, Konstantinos Bozinakis, Anastasios Kriebardis, Sofia Styliara, Aikaterini Karastathi, Nikolaos Farmakas, Maria Luiza Kraft Kohler Ribeiro, Ana Carolina Barcellos, Hannah Gabriele Ferreira Silva, Luís Henrique Mattei Carletto, Marcela Carolina Bet, Nathalia Zorze Rossetto, Nelson Augusto Rosario, Herberto Jose Chong-Neto, Fernanda Valença, Marina Novaes, Mariana Gomes, Carla Seifert, Alfredo Neto, Flavia Loyola, José Rios, Tatiana Silva, Aline Neves, Oznur Abadoglu, Bilun Gemicioglu, Hasan Bayram, Arif Cimrin, Levent Akyildiz, Aykut Cilli, Hakan Gunen, Tevfik Ozlu, Mecit Suerdem, Esra Uzaslan, Zeynep Misirligil, Snezana Ristic-Stojanovic, A. Milicevic, A. Milenkovic, Jelena Cvejic, Jelena Jankovic, Sanja Dimic-Janjic, Natasa Djurdjevic, Vladyslava Barzylovych, Tetiana Umanets, Anastasia Barzylovych, Karyn Winkler, Jessica Margarinos, Dylan Martin, Maja Nowakowski, Rauno Joks, Tsili Zangen, Olga Bernadsky, Mona Boaz, Gratiana Hermann, Rachel Aviv, Olga Kuperboim, Larisa Ramichanov, Efrat Broide, Raanan Shamir, Noam Zevit, Ron Shaoul, Alex Fich, Arie Levine, Isaac Melamed, Roopesh Singh Gangwar, Yael Minai-Fleminger, Mansour Seaf, Amichai Gutgold, Aarti Shikotra, Anoop Chauhan, Stephen Holgate, Peter Bradding, Peter Howarth, Ron Eliashar, Neville Berkman, Francesca Levi-Schaffer, Sung-il Woo, Betul Celik, Tangul Bulut, Arzu Didem Yalcin, Luiz Querino Caldas, Ronit Confino-Cohen, Yossi Rosman, Arnon Goldberg, Oded Breuer, Roopesh Singh, Ahlam Barhoum, Eitan Kerem, Tatiana Slavyanskaya, Revaz Sepiashvili, Elena A. Blinova, Ekaterina A. Pashkina, Marina I. Leonova, Vera M. Nepomnyaschikh, Darya V. Demina, Vladimir A. Kozlov, Revital Shamri, Kristen M. Young, Peter F. Weller, Rodolfo de Paula Vieira, Manoel Carneiro Oliveira-Junior, Nilsa Regina Damasceno-Rodrigues, Fernanda Magalhães Arantes-Costa, Milton Arruda Martins, Ana Paula Ligeiro Oliveira, Alfred Bernard, Antonia Sardella, Catherine Voisin, Simon Royce, Hamish Philpott, Sanjay Nandurkar, Francis Thien, Peter Gibson, Rodolfo Bianchini, Franziska Roth-Walter, Anna Ohradanova-Repic, Gerlinde Hofstetter, Ina Herrmann, Maria Isabel Carvalho, Karin Hufnagl, Erika Bajna, Georg Roth, Hannes Stockinger, Erika Jensen-Jarolim, Meital Almog, Aharon Kessel, Larisa Apov, Carlos Sanchez Salguero, Alvaro Sanchez Chacon, Abbos Nazarov, Shaxbos Ergashev, Irina Nesterova, Svetlana Kovaleva, Galina Chudilova, Ludmila Lomtatidze, Sarah De Schryver, Alizee Dery, Ann Clarke, Kari Nadeau, Kimberly Weatherall, Celia Greenwood, Denise Daley, Yuka Asai, Moshe Ben-Shoshan, Irina Balmasova, Elena Malova, Stefanie Wagner, Luis F. Pacios, Michael Wallner, Markus Wiederstein, Anna E. Tevs, Nataly Tataurshchikova, Baigalmaa Sangidorj, Anna Ronzhina, Manana Chikhladze, Oliver F. Wirz, Willem van de Veen, David Mirer, Hideaki Morita, Can Altunbulakli, Sebastian L. Johnston, Nicholas Glanville, Nikolaos G. Papadopoulos, Cezmi A. Akdis, Mübeccel Akdis, Avner Reshef, Marc Riedl, Vesna Grivcheva Panovska, Dumitru Moldovan, James Baker, William H. Yang, Sladjana Andrejevic, Richard F. Lockey, Roman Hakl, Shmuel Kivity, Luca Bellizzi, Joseph R. Harper, Anurag Relan, and Marco Cicardi

Subjects
Immunologic diseases. Allergy, RC581-607
Published
2017
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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. Acoustic metamaterials-driven transdermal drug delivery for rapid and on-demand management of acute disease.

Author

Xu, Junhua, Cai, Hongwei, Wu, Zhuhao, Li, Xiang, Tian, Chunhui, Ao, Zheng, Niu, Vivian C, Xiao, Xiao, Jiang, Lei, Khodoun, Marat, Rothenberg, Marc, Mackie, Ken, Chen, Jun, Lee, Luke P, and Guo, Feng

Subjects
Skin, Animals, Mice, Acute Disease, Drug Delivery Systems, Administration, Cutaneous, Acoustics, Female, Rare Diseases, Orphan Drug, Biotechnology, 5.1 Pharmaceuticals, Development of treatments and therapeutic interventions, Good Health and Well Being
Abstract

Transdermal drug delivery provides convenient and pain-free self-administration for personalized therapy. However, challenges remain in treating acute diseases mainly due to their inability to timely administrate therapeutics and precisely regulate pharmacokinetics within a short time window. Here we report the development of active acoustic metamaterials-driven transdermal drug delivery for rapid and on-demand acute disease management. Through the integration of active acoustic metamaterials, a compact therapeutic patch is integrated for penetration of skin stratum corneum and active percutaneous transport of therapeutics with precise control of dose and rate over time. Moreover, the patch device quantitatively regulates the dosage and release kinetics of therapeutics and achieves better delivery performance in vivo than through subcutaneous injection. As a proof-of-concept application, we show our method can reverse life-threatening acute allergic reactions in a female mouse model of anaphylaxis via a multi-burst delivery of epinephrine, showing better efficacy than a fixed dosage injection of epinephrine, which is the current gold standard 'self-injectable epinephrine' strategy. This innovative method may provide a promising means to manage acute disease for personalized medicine.

Published
2023

4. Caregiver worry about COVID-19 as a predictor of social mitigation behaviours and SARS-CoV-2 infection in a 12-city U.S. surveillance study of households with children

Author

Brunwasser, Steven M., Gebretsadik, Tebeb, Satish, Anisha, Cole, Jennifer C., Dupont, William D., Joseph, Christine, Bendixsen, Casper G., Calatroni, Agustin, Arbes, Samuel J., Jr, Fulkerson, Patricia C., Sanders, Joshua, Bacharier, Leonard B., Camargo, Jr, Carlos A., Johnson, Christine Cole, Furuta, Glenn T., Gruchalla, Rebecca S., Gupta, Ruchi S., Khurana Hershey, Gurjit K., Jackson, Daniel J., Kattan, Meyer, Liu, Andrew, O'Connor, George T., Rivera-Spoljaric, Katherine, Phipatanakul, Wanda, Rothenberg, Marc E., Seibold, Max A., Seroogy, Christine M., Teach, Stephen J., Zoratti, Edward M., Togias, Alkis, and Hartert, Tina V.

Published
2025
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5. Harnessing Artificial Intelligence to Infer Novel Spatial Biomarkers for the Diagnosis of Eosinophilic Esophagitis

Author

Larey, Ariel, Aknin, Eliel, Daniel, Nati, Osswald, Garrett A., Caldwell, Julie M., Rochman, Mark, Wasserman, Tanya, Collins, Margaret H., Arva, Nicoleta C., Yang, Guang-Yu, Rothenberg, Marc E., and Savir, Yonatan

Subjects
Computer Science - Artificial Intelligence, Computer Science - Computer Vision and Pattern Recognition, Quantitative Biology - Quantitative Methods
Abstract

Eosinophilic esophagitis (EoE) is a chronic allergic inflammatory condition of the esophagus associated with elevated esophageal eosinophils. Second only to gastroesophageal reflux disease, EoE is one of the leading causes of chronic refractory dysphagia in adults and children. EoE diagnosis requires enumerating the density of esophageal eosinophils in esophageal biopsies, a somewhat subjective task that is time-consuming, thus reducing the ability to process the complex tissue structure. Previous artificial intelligence (AI) approaches that aimed to improve histology-based diagnosis focused on recapitulating identification and quantification of the area of maximal eosinophil density. However, this metric does not account for the distribution of eosinophils or other histological features, over the whole slide image. Here, we developed an artificial intelligence platform that infers local and spatial biomarkers based on semantic segmentation of intact eosinophils and basal zone distributions. Besides the maximal density of eosinophils (referred to as Peak Eosinophil Count [PEC]) and a maximal basal zone fraction, we identify two additional metrics that reflect the distribution of eosinophils and basal zone fractions. This approach enables a decision support system that predicts EoE activity and classifies the histological severity of EoE patients. We utilized a cohort that includes 1066 biopsy slides from 400 subjects to validate the system's performance and achieved a histological severity classification accuracy of 86.70%, sensitivity of 84.50%, and specificity of 90.09%. Our approach highlights the importance of systematically analyzing the distribution of biopsy features over the entire slide and paves the way towards a personalized decision support system that will assist not only in counting cells but can also potentially improve diagnosis and provide treatment prediction., Comment: AL, EA, and ND have contributed equally to this work and share first authorship. YS is the corresponding author, e-mail: yoni.savir@technion.ac.il

Published
2022

6. 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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8. Long-term durability between parent and child patient-reported outcomes in eosinophilic esophagitis

Author

Martin, Lisa J., Zhang, Xue, Chehade, Mirna, Davis, Carla M., Dellon, Evan S., Falk, Gary W., Gupta, Sandeep K., Hirano, Ikuo, Hiremath, Girish S., Katzka, David A., Khoury, Paneez, Leung, John, Menard-Katcher, Paul, Gonsalves, Nirmala, Pesek, Robert D., Spergel, Jonathan M., Wechsler, Joshua B., Kliewer, Kara, Arva, Nicoleta C., Collins, Margaret H., Pletneva, Maria, Yang, Guang-Yu, Furuta, Glenn T., Rothenberg, Marc E., and Aceves, Seema S.

Published
2024
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11. 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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12. 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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17. PECNet: A Deep Multi-Label Segmentation Network for Eosinophilic Esophagitis Biopsy Diagnostics

Author

Daniel, Nati, Larey, Ariel, Aknin, Eliel, Osswald, Garrett A., Caldwell, Julie M., Rochman, Mark, Collins, Margaret H., Yang, Guang-Yu, Arva, Nicoleta C., Capocelli, Kelley E., Rothenberg, Marc E., and Savir, Yonatan

Subjects
Computer Science - Computer Vision and Pattern Recognition, Computer Science - Machine Learning, Electrical Engineering and Systems Science - Image and Video Processing, Quantitative Biology - Quantitative Methods
Abstract

Background. Eosinophilic esophagitis (EoE) is an allergic inflammatory condition of the esophagus associated with elevated numbers of eosinophils. Disease diagnosis and monitoring requires determining the concentration of eosinophils in esophageal biopsies, a time-consuming, tedious and somewhat subjective task currently performed by pathologists. Methods. Herein, we aimed to use machine learning to identify, quantitate and diagnose EoE. We labeled more than 100M pixels of 4345 images obtained by scanning whole slides of H&E-stained sections of esophageal biopsies derived from 23 EoE patients. We used this dataset to train a multi-label segmentation deep network. To validate the network, we examined a replication cohort of 1089 whole slide images from 419 patients derived from multiple institutions. Findings. PECNet segmented both intact and not-intact eosinophils with a mean intersection over union (mIoU) of 0.93. This segmentation was able to quantitate intact eosinophils with a mean absolute error of 0.611 eosinophils and classify EoE disease activity with an accuracy of 98.5%. Using whole slide images from the validation cohort, PECNet achieved an accuracy of 94.8%, sensitivity of 94.3%, and specificity of 95.14% in reporting EoE disease activity. Interpretation. We have developed a deep learning multi-label semantic segmentation network that successfully addresses two of the main challenges in EoE diagnostics and digital pathology, the need to detect several types of small features simultaneously and the ability to analyze whole slides efficiently. Our results pave the way for an automated diagnosis of EoE and can be utilized for other conditions with similar challenges.

Published
2021

21. Machine learning approach for biopsy-based identification of eosinophilic esophagitis reveals importance of global features

Author

Czyzewski, Tomer, Daniel, Nati, Rochman, Mark, Caldwell, Julie M., Osswald, Garrett A., Collins, Margaret H., Rothenberg, Marc E., and Savir, Yonatan

Subjects
Computer Science - Computer Vision and Pattern Recognition, Computer Science - Machine Learning, Electrical Engineering and Systems Science - Image and Video Processing, Quantitative Biology - Quantitative Methods
Abstract

Goal: Eosinophilic esophagitis (EoE) is an allergic inflammatory condition characterized by eosinophil accumulation in the esophageal mucosa. EoE diagnosis includes a manual assessment of eosinophil levels in mucosal biopsies - a time-consuming, laborious task that is difficult to standardize. One of the main challenges in automating this process, like many other biopsy-based diagnostics, is detecting features that are small relative to the size of the biopsy. Results: In this work, we utilized hematoxylin- and eosin-stained slides from esophageal biopsies from patients with active EoE and control subjects to develop a platform based on a deep convolutional neural network (DCNN) that can classify esophageal biopsies with an accuracy of 85%, sensitivity of 82.5%, and specificity of 87%. Moreover, by combining several downscaling and cropping strategies, we show that some of the features contributing to the correct classification are global rather than specific, local features. Conclusions: We report the ability of artificial intelligence to identify EoE using computer vision analysis of esophageal biopsy slides. Further, the DCNN features associated with EoE are based on not only local eosinophils but also global histologic changes. Our approach can be used for other conditions that rely on biopsy-based histologic diagnostics.

Published
2021

22. Single cell transcriptomic analysis of HPV16-infected epithelium identifies a keratinocyte subpopulation implicated in cancer

Author

Bedard, Mary C., Chihanga, Tafadzwa, Carlile, Adrean, Jackson, Robert, Brusadelli, Marion G., Lee, Denis, VonHandorf, Andrew, Rochman, Mark, Dexheimer, Phillip J., Chalmers, Jeffrey, Nuovo, Gerard, Lehn, Maria, Williams, David E. J., Kulkarni, Aditi, Carey, Molly, Jackson, Amanda, Billingsley, Caroline, Tang, Alice, Zender, Chad, Patil, Yash, Wise-Draper, Trisha M., Herzog, Thomas J., Ferris, Robert L., Kendler, Ady, Aronow, Bruce J., Kofron, Matthew, Rothenberg, Marc E., Weirauch, Matthew T., Van Doorslaer, Koenraad, Wikenheiser-Brokamp, Kathryn A., Lambert, Paul F., Adam, Mike, Steven Potter, S., and Wells, Susanne I.

Published
2023
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23. A novel class of TMPRSS2 inhibitors potently block SARS-CoV-2 and MERS-CoV viral entry and protect human epithelial lung cells

Author

Mahoney, Matthew, Damalanka, Vishnu C, Tartell, Michael A, Chung, Dong hee, Lourenço, André Luiz, Pwee, Dustin, Bridwell, Anne E Mayer, Hoffmann, Markus, Voss, Jorine, Karmakar, Partha, Azouz, Nurit P, Klingler, Andrea M, Rothlauf, Paul W, Thompson, Cassandra E, Lee, Melody, Klampfer, Lidija, Stallings, Christina L, Rothenberg, Marc E, Pöhlmann, Stefan, Whelan, Sean PJ, O’Donoghue, Anthony J, Craik, Charles S, and Janetka, James W

Subjects
Biological Sciences, Medicinal and Biomolecular Chemistry, Chemical Sciences, Lung, Coronaviruses Therapeutics and Interventions, Emerging Infectious Diseases, Orphan Drug, Pneumonia & Influenza, Rare Diseases, Pneumonia, Coronaviruses, Infectious Diseases, 5.1 Pharmaceuticals, Respiratory, Animals, Benzamidines, Benzothiazoles, COVID-19, Cell Line, Drug Design, Epithelial Cells, Esters, Guanidines, Humans, Mice, Middle East Respiratory Syndrome Coronavirus, Oligopeptides, SARS-CoV-2, Serine Endopeptidases, Small Molecule Libraries, Substrate Specificity, Virus Internalization, COVID-19 Drug Treatment, antiviral, protease inhibitor, structure-based drug discovery, PS-SCL
Abstract

The host cell serine protease TMPRSS2 is an attractive therapeutic target for COVID-19 drug discovery. This protease activates the Spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and of other coronaviruses and is essential for viral spread in the lung. Utilizing rational structure-based drug design (SBDD) coupled to substrate specificity screening of TMPRSS2, we have discovered covalent small-molecule ketobenzothiazole (kbt) TMPRSS2 inhibitors which are structurally distinct from and have significantly improved activity over the existing known inhibitors Camostat and Nafamostat. Lead compound MM3122 (4) has an IC50 (half-maximal inhibitory concentration) of 340 pM against recombinant full-length TMPRSS2 protein, an EC50 (half-maximal effective concentration) of 430 pM in blocking host cell entry into Calu-3 human lung epithelial cells of a newly developed VSV-SARS-CoV-2 chimeric virus, and an EC50 of 74 nM in inhibiting cytopathic effects induced by SARS-CoV-2 virus in Calu-3 cells. Further, MM3122 blocks Middle East respiratory syndrome coronavirus (MERS-CoV) cell entry with an EC50 of 870 pM. MM3122 has excellent metabolic stability, safety, and pharmacokinetics in mice, with a half-life of 8.6 h in plasma and 7.5 h in lung tissue, making it suitable for in vivo efficacy evaluation and a promising drug candidate for COVID-19 treatment.

Published
2021

25. 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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26. Development of the Pediatric Quality of Life Inventory™ Eosinophilic Esophagitis Module items: qualitative methods

Author

Franciosi James P, Hommel Kevin A, Greenberg Allison B, DeBrosse Charles W, Greenler Alexandria J, Abonia J Pablo, Rothenberg Marc E, and Varni James W

Subjects
Quality of life, Eosinophilic Esophagitis, Children, PedsQL™, Pediatrics, Diseases of the digestive system. Gastroenterology, RC799-869
Abstract

Abstract Background Currently there is no disease-specific outcome measure to assess the health-related quality of life (HRQOL) of pediatric patients with Eosinophilic Esophagitis (EoE). Therefore, the objective of this qualitative study was to further develop and finalize the items and support the content validity for the new Pediatric Quality of Life Inventory™ (PedsQL™) Eosinophilic Esophagitis Module. Methods Multiphase qualitative methodology was utilized in the development of the PedsQL™ EoE Module conceptual model. Focus interview transcripts of pediatric patients with EoE and their parents and expert review were previously used to develop the initial items and domains for the PedsQL™ EoE Module. In the current investigation, utilizing the respondent debriefing methodology, cognitive interviewing was conducted individually with pediatric patients with EoE and their parents on each newly developed item. Results Information from a total of 86 participants was obtained in combination from the previous investigation and the current study. From the previous 42 focus interviews, items were developed around the domain themes of symptoms, difficulties with eating food, treatment adherence, worry about symptoms and illness, feelings of being different than family and peers, and problems discussing EoE with others. In the current study’s cognitive interviewing phase, a separate cohort of 44 participants systematically reviewed and provided feedback on each item. Items were added, modified or deleted based on this feedback. Items were finalized after this feedback from patients and parents. Conclusions Using well-established qualitative methods, the content validity of the new PedsQL™ Eosinophilic Esophagitis Module items was supported in the current investigation. In the next iterative instrument development phase, the PedsQL™ Eosinophilic Esophagitis Module is now undergoing multisite national field testing.

Published
2012
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27. Development of a validated patient-reported symptom metric for pediatric Eosinophilic Esophagitis: qualitative methods

Author

Franciosi James P, Hommel Kevin A, DeBrosse Charles W, Greenberg Allison B, Greenler Alexandria J, Abonia J Pablo, Rothenberg Marc E, and Varni James W

Subjects
Diseases of the digestive system. Gastroenterology, RC799-869
Abstract

Abstract Background Previous attempts to measure symptoms in pediatric Eosinophilic Esophagitis (EoE) have not fully included patients and parents in the item development process. We sought to identify and validate key patient self-reported and parent proxy-reported outcomes (PROs) specific to EoE. Methods We developed methodology for focus and cognitive interviews based on the Food and Drug Administration (FDA) guidelines for PROs, the validated generic PedsQL™ guidelines, and the consolidated criteria for reporting qualitative research (COREQ). Both child (ages 8-12 and 13-18) and parent-proxy (ages 2-4, 5-7, 8-12, and 13-18) interviews were conducted. Results We conducted 75 interviews to construct the new instrument. Items were identified and developed from individual focus interviews, followed by cognitive interviews for face and content validation. Initial domains of symptom frequency and severity were developed, and open-ended questions were used to generate specific items during the focus interviews. Once developed, the instrument construct, instructions, timeframe, scoring, and specific items were systematically reviewed with a separate group of patients and their parents during the cognitive interviews. Conclusions To capture the full impact of pediatric EoE, both histologic findings and PROs need to be included as equally important outcome measures. We have developed the face and content validated Pediatric Eosinophilic Esophagitis Symptom Score (PEESS™ v2.0). The PEESS™ v2.0 metric is now undergoing multisite national field testing as the next iterative instrument development phase.

Published
2011
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28. 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

29. The cationic amino acid transporter 2 is induced in inflammatory lung models and regulates lung fibrosis

Author

Rothenberg Marc E, Ellies Lesley G, Chiaramonte Monica G, Niese Kathryn A, and Zimmermann Nives

Subjects
Diseases of the respiratory system, RC705-779
Abstract

Abstract Background Arginine is an amino acid that serves as a substrate for the enzymes nitric oxide synthase (NOS) and arginase, leading to synthesis of NO and ornithine, respectively. As such, arginine has the potential to influence diverse fundamental processes in the lung. Methods We used mice deficient in cationic amino acid transporter (CAT) 2 in models of allergic airway inflammation and pulmonary fibrosis. Results We report that the arginine transport protein CAT2 was over-expressed in the lung during the induction of allergic airway inflammation. Furthermore, CAT2 mRNA was strongly induced by transgenically over-expressed IL-4, and allergen-induced expression was dependent upon signal-transducer-and-activator-of-transcription (STAT) 6. In situ mRNA hybridization demonstrated marked staining of CAT2, predominantly in scattered mononuclear cells. Analysis of allergic airway inflammation and bleomycin-induced inflammation in CAT2-deficient mice revealed that while inflammation was independent of CAT2 expression, bleomycin-induced fibrosis was dependent upon CAT2. Mechanistic analysis revealed that arginase activity in macrophages was partly dependent on CAT2. Conclusion Taken together, these results identify CAT2 as a regulator of fibrotic responses in the lung.

Published
2010
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31. Bone marrow cell derived arginase I is the major source of allergen-induced lung arginase but is not required for airway hyperresponsiveness, remodeling and lung inflammatory responses in mice

Author

Rothenberg Marc E, Wills-Karp Marsha, O'Brien William E, Cederbaum Stephen D, Hajek Amanda R, Collier Ann R, Niese Kathryn A, and Zimmermann Nives

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background Arginase is significantly upregulated in the lungs in murine models of asthma, as well as in human asthma, but its role in allergic airway inflammation has not been fully elucidated in mice. Results In order to test the hypothesis that arginase has a role in allergic airway inflammation we generated arginase I-deficient bone marrow (BM) chimeric mice. Following transfer of arginase I-deficient BM into irradiated recipient mice, arginase I expression was not required for hematopoietic reconstitution and baseline immunity. Arginase I deficiency in bone marrow-derived cells decreased allergen-induced lung arginase by 85.8 ± 5.6%. In contrast, arginase II-deficient mice had increased lung arginase activity following allergen challenge to a similar level to wild type mice. BM-derived arginase I was not required for allergen-elicited sensitization, recruitment of inflammatory cells in the lung, and proliferation of cells. Furthermore, allergen-induced airway hyperresponsiveness and collagen deposition were similar in arginase-deficient and wild type mice. Additionally, arginase II-deficient mice respond similarly to their control wild type mice with allergen-induced inflammation, airway hyperresponsiveness, proliferation and collagen deposition. Conclusion Bone marrow cell derived arginase I is the predominant source of allergen-induced lung arginase but is not required for allergen-induced inflammation, airway hyperresponsiveness or collagen deposition.

Published
2009
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32. Breakthroughs in understanding and treating eosinophilic gastrointestinal diseases presented at the CEGIR/TIGERs Symposium at the 2022 American Academy of Allergy, Asthma & Immunology Meeting

Author

Chehade, Mirna, Wright, Benjamin L., Atkins, Dan, Aceves, Seema S., Ackerman, Steven J., Assa’ad, Amal H., Bauer, Maureen, Collins, Margaret H., Commins, Scott P., Davis, Carla M., Dellon, Evan S., Doerfler, Bethan, Gleich, Gerald J., Gupta, Sandeep K., Hill, David A., Jensen, Elizabeth T., Katzka, David, Kliewer, Kara, Kodroff, Ellyn, Kottyan, Leah C., Kyle, Shay, Muir, Amanda B., Pesek, Robert D., Peterson, Kathryn, Shreffler, Wayne G., Spergel, Jonathan M., Strobel, Mary Jo, Wechsler, Joshua, Zimmermann, Nives, Furuta, Glenn T., and Rothenberg, Marc E.

Published
2023
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33. Efficacy and safety of dupilumab up to 52 weeks in adults and adolescents with eosinophilic oesophagitis (LIBERTY EoE TREET study): a multicentre, double-blind, randomised, placebo-controlled, phase 3 trial

Author

Rothenberg, Marc E, Dellon, Evan S, Collins, Margaret H, Hirano, Ikuo, Chehade, Mirna, Bredenoord, Albert J, Lucendo, Alfredo J, Spergel, Jonathan M, Sun, Xian, Hamilton, Jennifer D, Mortensen, Eric, Laws, Elizabeth, Maloney, Jennifer, Mannent, Leda P, McCann, Eilish, Liu, Xia, Glotfelty, Lila, and Shabbir, Arsalan

Published
2023
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34. 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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35. 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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36. Advancing patient care through the Consortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR)

Author

Aceves, Seema, Collins, Margaret H, Rothenberg, Marc E, Furuta, Glenn T, Gonsalves, Nirmala, Researchers, Consortium of Eosinophilic Gastrointestinal Disease, Abonia, J Pablo, 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, 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, Paliana, Allisa, Pan, Zhaoxing, Pesek, Robbie, Peterson, Kathryn, Poppendeck, Heidi, Putnam, Philip, Rivera, Fabian, Rothenberg, Marc, Rudman-Spergel, Amanda, Sable, Kathleen, Schoepfer, Alain, Scott, Melissa, Sheridan, Rachel, Sinanovic, Selma, Spergel, Jonathan, Strobel, MaryJo, and Sun, Kiki

Subjects
Biomedical and Clinical Sciences, Immunology, Clinical Research, Digestive Diseases, Clinical Trials and Supportive Activities, Evaluation of treatments and therapeutic interventions, Detection, screening and diagnosis, 6.9 Resources and infrastructure (treatment evaluation), 4.5 Resources and infrastructure (detection), Good Health and Well Being, Biomedical Research, Clinical Trials as Topic, Enteritis, Eosinophilia, Eosinophilic Esophagitis, Gastritis, National Institutes of Health (U.S.), United States, Eosinophils, gastrointestinal, consortium, allergy, esophagitis, advocacy, Consortium of Eosinophilic Gastrointestinal Disease Researchers, Allergy
Abstract

Recent advances in rare disease research are accelerated by the work of consortia that have been supported by the National Institutes of Health. Development of such consortia rely on multidisciplinary relationships and engagement with patient advocacy groups, as well as the National Institutes of Health and industry and academic partners. In this rostrum we present the development of such a process that focuses on eosinophilic gastrointestinal diseases. Principal investigators, patient advocacy groups, research assistants, and trainees work together to perform natural history studies that promote clinical trial readiness tools, conduct clinical trials, train a new generation of investigators, and perform innovative pilot studies.

Published
2020

37. Analysis of the CCR3 promoter reveals a regulatory region in exon 1 that binds GATA-1

Author

Koch Laura E, Colyer Jessica L, Zimmermann Nives, and Rothenberg Marc E

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background CC Chemokine Receptor 3 (CCR3), the major chemokine receptor expressed on eosinophils, binds promiscuously to several ligands including eotaxins 1, 2, and 3. Even though the only cells that consistently accumulate following eotaxin administration in vivo are myeloid cells (primarily eosinophils), other cell types have recently been shown to express CCR3. It is therefore important to elucidate the molecular mechanisms regulating receptor expression. Results In order to define regions responsible for CCR3 transcription, a DNAse hypersensitive site was identified in the vicinity of exon 1. Coupled with our previous data implicating exon 1 in CCR3 transcription, we hypothesized that transcription factors bind to exon-1. Electrophoretic mobility shift analysis revealed that nuclear proteins in eosinophilic cells bound to exon 1. Furthermore, antibody interference and mutation studies demonstrated GATA-1 binding to exon 1. In order to test the 1.6-kb CCR3 promoter element (that includes exon 1) for in vivo function, this region was used to generate transgenic mice that expressed a reporter protein. Strong transgene expression was achieved, with the pattern of expression suggesting a broad acting promoter. Conclusion The transcription factor GATA-1 binds to CCR3 exon 1. The 1.6-kb CCR3 promoter element, that includes exon 1, is a strong promoter in vivo.

Published
2005
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38. 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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41. Development of a Practical Guide to Implement and Monitor Diet Therapy for Eosinophilic Esophagitis

Author

Aceves, Seema S., Abonia, Pablo, Atkins, Dan, Bonis, Peter A., Chehade, Mirna, Falk, Gary W., Furuta, Glenn T., Gupta, Sandeep K., Kagalwalla, Amir F., Kodroff, Ellyn, Kyle, Scholeigh, Leung, John, Menard-Katcher, Paul, Mir, Sabina, Mukkada, Vincent A., Pesek, Robert, Rothenberg, Marc E., Spergel, Jonathan M., Strobel, Mary Jo, Wechsler, Joshua B., Chang, Joy W., Kliewer, Kara, Haller, Emily, Lynett, Amanda, Doerfler, Bethany, Katzka, David A., Peterson, Kathryn A., Dellon, Evan S., and Gonsalves, Nirmala

Published
2023
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42. 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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44. 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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46. Genome-wide admixture and association analysis identifies African ancestry–specific risk loci of eosinophilic esophagitis in African Americans

Author

Wechsler, Joshua, Davis, Carla, Furuta, Glenn, Khoury, Paneez, Aceves, Seema, Gupta, Sandeep K., Spergel, Jonathan, Leung, John, Menard-Katcher, Paul, Falk, Gary, Hirano, Ikuo, Gonsalves, Nirmala Prabu, Peterson, Kathryn, Gautam, Yadu, Caldwell, Julie, Kottyan, Leah, Chehade, Mirna, Dellon, Evan S., Rothenberg, Marc E., and Mersha, Tesfaye B.

Published
2023
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48. High Discovery Rate of Duodenal and Gastric Eosinophilia in Patients With Unexplained Moderate–Severe Abdominal Symptoms: A Prospective US Multisite Study

Author

Talley, Nicholas J., Peterson, Kathryn A., Genta, Robert M., Chang, Alan T., Dellon, Evan S., Sandborn, William J., Lacy, Brian E., Chehade, Mirna, Hirano, Ikuo, Gonsalves, Nirmala, Lembo, Anthony, Schmitt, Colleen M., Rothenberg, Marc E., Jain, Neal, Pletneva, Maria A., Turner, Kevin O., and Youngblood, Bradford A.

Published
2023
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49. The role of biologics in pediatric food allergy and eosinophilic gastrointestinal disorders

Author

Sindher, Sayantani B., Barshow, Suzanne, Tirumalasetty, Jyothi, Arasi, Stefania, Atkins, Dan, Bauer, Maureen, Bégin, Philippe, Collins, Margaret H., Deschildre, Antoine, Doyle, Alfred D., Fiocchi, Alessandro, Furuta, Glenn T., Garcia-Lloret, Maria, Mennini, Maurizio, Rothenberg, Marc E., Spergel, Jonathan M., Wang, Julie, Wood, Robert A., Wright, Benjamin L., Zuberbier, Torsten, Chin, Andrew R., Long, Andrew, Nadeau, Kari C., and Chinthrajah, R. Sharon

Published
2023
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