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Hegazy lab

Host-Microbiota interactions shape intestinal inflammation

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Selected publications

Inflammatory Mechanisms

The gastrointestinal tract contains a huge number of immune cells and harbours a large population of bacteria that exist in a symbiotic relationship with the host. In inflammatory bowel disease (IBD) this balance is perturbed, triggering pro-inflammatory responses that drive disease symptoms. Our work focuses on untangling the interplay between the host and microbiota during inflammation.

We have several diverse projects running with the common aim of identifying novel inflammatory signatures that may be amenable to therapeutic blockade, or be predictive markers of treatment failure. We wish to examine the link between bacterial opsonisation by the immune system and the CD4+ T cell responses to these bacteria, with the aim of identifying pathogenic and protective T cell signatures. Previous work has identified a novel role for oncostatin M (OSM) in mice and humans. Upregulation of OSM was found to be a predictive marker for anti-TNF treatment failure in IBD and blockade of OSM in vivo ameliorated disease symptoms in a mouse model of colitis. Therefore, we wish to exploit dysbiosis- and genetic-driven IBD mouse models and primary human tissue samples to explore the impact of OSM on intestinal epithelial cells and barrier functions in health and disease.

A comprehensive understanding of how the microbiota-immune system crosstalk is perturbed in chronic inflammation is essential, particularly in light of the high rate of treatment failure. Using a combination of mouse and human T cell immunology, mucosal immunology and animal models of disease as well as clinical specimens and sequence based approaches, we aim to identify environmental, microbial and inflammatory drivers that promote maladaptation and gut tissue inflammation. Our focus on clinical samples ensure that the work we carry out is of high relevance to patients and increases the likelihood of us delivering findings of future clinical relevance.

Inflammatory Mechanisms Prof. Dr. med. Dr. rer. nat. Ahmed N. Hegazy Phone +49-30-450 514 343 ahmed.hegazy@charite.de more
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Group leader
Prof. Ahmed Hegazy, M.D., Ph.D.

Veronika Horn, MD

Ph.D. students
Zuzanna Borek, Msc
Roodline Cineus, Msc
Yu-hsin hsieh, Msc

M.Sc. Students:
Saskia Hainbuch
Elena von Coburg
Ravi Shankar Ojha

MD students:
Aya abdel Rahman

Diana Boesel, RA

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  • Andreas Bergthaler, Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria
  • Sylvia Duncan and Alan Walker, Rowett Institute of Nutrition and Health, University of Aberdeen, Aberdeen, United Kingdom.
  • Lukas Flatz, Klinik für Dermatologie, Venerologie und Allergologie und Institut für Immunbiologie, Kantonsspital St. Gallen, Switzerland
  • Max Löhning, Pitzer-Labor Arthroseforschung, Med. Klinik m.S. Rheumatologie u. Klin. Immunologie, Charité – Universitätsmedizin Berlin (CCM)
  • Mir-Farzin Mashreghi, Koji Tokoyoda and Hyun-Dong Chang, Deutsches Rheuma-Forschungszentrum-Berlin
  • Gerhard Mueller-Newen, Institute of Biochemistry and Molecular Biology, RWTH Aachen University, Aachen, Germany.
  • Thomas Schneider, Klinik für Gastroenterologie, Infektiologie und Rheumatologie, Charité – Universitätsmedizin Berlin (CBF)
  • Britta Siegmund, Klinik für Gastroenterologie, Infektiologie und Rheumatologie, Charité – Universitätsmedizin Berlin (CBF)
  • Sarah Teichmann and Mike Stubbington, Wellcome Trust Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, United Kingdom
  • Nathaniel West, Genetech, San Francisco, United States
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Continue to Selected publications
  • Berner, F., Bomze, D., Diem, S., Ali, O.H., Fässler, M., Ring, S., Niederer, R., Ackermann, C.J., Baumgaertner, P., Pikor, N., Cruz, C.G., van de Veen, W., Akdis, M., Nikolaev, S., Läubli, H., Zippelius, A., Hartmann, F., Cheng, H.-W., Hönger, G., Recher, M., Goldman, J., Cozzio, A., Früh, M., Neefjes, J., Driessen, C., Ludewig, B., Hegazy, A.N., Jochum, W., Speiser, D.E., Flatz, L., 2019. Association of Checkpoint Inhibitor-Induced Toxic Effects With Shared Cancer and Tissue Antigens in Non-Small Cell Lung Cancer. JAMA Oncol. ePub April 25.
  • Stockenhuber, K., Hegazy, A.N., West, N.R., Ilott, N.E., Stockenhuber, A., Bullers, S.J., Thornton, E.E., Arnold, I.C., Tucci, A., Waldmann, H., Ogg, G.S., Powrie, F., 2018. Foxp3+ T reg cells control psoriasiform inflammation by restraining an IFN-I-driven CD8+ T cell response. Journal of Experimental Medicine 215, 1987–1998.
  • West, N.R., Owens, B.M.J., Hegazy, A.N., 2018. The oncostatin M-stromal cell axis in health and disease. Scand J Immunol 176, e12694.
  • Hegazy* A.N., West* N.R., Stubbington, M.J.T., Wendt E., Suijker, K., Datsi, A., This, S., Danne, C., Campion, S., Duncan, S.H., Owens, B.M.J., Uhlig, H.H., McMichael, A., Oxford IBD Cohort Investigators, 
Bergthaler, A., Teichmann, S.A., Keshav, S., Powrie, F., 2017. Gut Microbiota Induce Local And Systemic CD4 T Cell Responses In Healthy Individuals That Are Altered In Inflammatory Bowel Diseases. Gastroenterology 153(5):1320-1337  (IF 16.8, cited 5)
  • Hegazy*N., West* N.R., Owens B.M.J., Görtz D., This S., Ryzhakov G., Bullers S., Rahman N., Owens R., Müller-Newen G., Powrie F., 2017. Oncostatin M drives intestinal inflammation in mice and its abundance 
predicts response to tumor necrosis factor-neutralizing therapy in 
patients with inflammatory bowel disease. Nat Med 23(5):579-589 (IF 32.6, cited 17)
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