Leitung

Prof. Dr. Dirk Haller CV

TRACK RECORD AND ACHIEVEMENT SUMMARY

Nutrition and the intestinal microbiome are key environmental factors in the aetiology of chronic disorders in the industrialized world. My whole scientific career is dedicated to develop a fundamental understanding of how the community of intestinal microbes contribute to inflammatory diseases (Renz, 2011 Nature Immunology; Metwaly, 2022 and 2025 Nat. Rev. Gastroenterol. Hepatol.). I pioneered the idea that commensal bacteria trigger a regulated circuit of inflammatory host responses through the integration of signals at the intestinal epithelial interface (Haller, 2000 Gut; Haller, 2002 J. Biol. Chem.; Shkoda, 2007 Gastroenterology), supporting a paradigm shift in the understanding of microbiome-host interactions. Over the last decades, my team and I identified protective and pro-inflammatory molecular structures of commensal bacteria (Steck, 2011 Gastroenterology; von Schillde, 2012 Cell Host & Microbe), and applied Koch’s postulates in germ-free mouse models to confirm their causal role in shaping inflammatory bowel diseases (IBD) (Schaubeck, 2016 Gut; Metwaly, 2020 Nature Communications). In order to broaden the breadth of microbiome research towards human translation, we employ clinical and population studies to specify the role of nutrition in modulating microbiome-related human health (Häcker, 2024 Cell Host & Microbe; Heppner, 2024 Cell Host & Microbe; Reitmeier, 2020 Cell Host & Microbe; Bazanella, 2018 Am. J. Clin. Nutrition; Lee, 2017 Gut). How is the complex repertoire of nutritional and microbial signals integrated at the intestinal interface to shape health and diseases (Rath, 2018 Nat. Rev. Gastroenterol. Hepatol.). We pioneered the intriguing new concept that metabolic disruption in the intestinal epithelium contribute to tissue pathology (Rath, 2011 Gut; Khaloian, 2020 Gut) and coined the concept of metabolic injury (Berger, 2016 Nature Communications; Urbauer, 2024 Cell Host & Microbe). Chronic inflammation and cancer development are tightly connected, and current research expands the concept of metabolic stress to cancer risk targeting long-chain fatty acid-mediated dysbiosis (Yan, 2017 Cancer Cell; Coleman, 2018 Gastroenterology; Coleman, Nature Metabolism 2025). A key emphasis of this exiting research is to explore novel therapeutic applications for nutritional and microbiome-related therapies. Receiving the distinguished Research Award of the United European Gastroenterology Association in 2021 and the recognition as Highly Cited Scientist in 2024 underlines my international visibility.  

SELECTED PUBLICATIONS

*Corresponding author

A complete list of publications is retrievable at http://orcid.org/0000-0002-6977-4085

(Scopus: N=261, h-index 75; Google Scholar: h-index 86). 

1. Coleman O., Sorbie A., Riva A., von Stern M., Kuhls S., Selegato D.M., Siegert L., Keidel I., Köhler N., Wirbel J., Kacprowski T., Dunkel A., Pauling J.K., Plagge J., Mediel-Cuadra D., Wagner S., Chadly I., Bierwith S., Peng T., Metzler T., Li X., Heikenwälder M., Schafmayer C., Hinz S., Röder C., Röcken C., Zimmermann M., Rosenstiel P., Steiger K., Jesinghaus M., Liebisch G., Ecker J., Schmidt C., Zeller G., Janssen K.P., and Haller D.* (2025) ATF6 activation alters colonic lipid metabolism causing tumor-associated microbial adaptation. Nature Metabolism (in press)

2. Metwaly A., Kriaa A., Hassani Z., Carraturo F., Druart C., Consortium I., Arnauts K., Wilmes P., Walter J., Rosshart S., Desai M.S., Dore J., Blottiere H.M. Maguin E., and Haller D.* (2025) A Consensus Statement on establishing causality, therapeutic applications and the use of preclinical models in microbiome research. Nature Reviews Gastroenterology and Hepatology doi: 10.1038/s41575-025-01041-3. 

3. Urbauer E., Aguanno D., Mindermann N., Omer H., Metwaly A., Krammel T., Faro T., Remke M., Reitmeier S., Bärthel S., Kersting J., Huang Z., Xian F., Schmidt M., Saur D., Huber S., Stecher B., List M., Gómez-Varela D., Steiger K., Allez M., Rath E., and Haller D.* (2024). Mitochondrial perturbation in the intestine causes microbiota-dependent injury and gene signatures discriminative of inflammatory disease. Cell Host and Microbe 32, 1347-1364

4. Heppner N., Reitmeier S., Heddes M., Merino M.V., Schwartz L., Dietrich A., List M., Gigl M., Meng C., Van Der Veen D.R., Schirmer M., Kleigrewe K., Omer H., Kiessling S., and Haller D.* (2024). Diurnal rhythmicity of infant fecal microbiota and metabolites: A randomized controlled interventional trial with infant formula. Cell Host and Microbe 32, 573-587

5. Häcker D., Siebert K., Smith B.J., Köhler N., Riva A., Mahapatra A., Heimes H., Nie J., Metwaly A., Hölz H., Manz Q., De Zen F., Heetmeyer J., Socas K., Le Thi G., Meng C., Kleigrewe K., Pauling J.K., Neuhaus K., List M., Pollard K.S., Schwerd T.*, and Haller D.* (2024). Exclusive enteral nutrition initiates individual protective microbiome changes to induce remission in pediatric Crohn's disease. Cell Host and Microbe 32, 2019-2034.

6. Metwaly A., Reitmeier S., and Haller D.* (2022). Microbiome risk profiles as biomarkers for inflammatory and metabolic disorders. Nature Reviews Gastroenterology and Hepatology 19, 383-397. 

7. Reitmeier S., Kiessling S., Clavel T., List M., Almeida E.L., Ghosh T.S., Neuhaus K., Grallert H., Linseisen J., Skurk T., Brandl B., Breuninger T.A., Troll M., Rathmann W., Linkohr B., Hauner H., Laudes M., Franke A., Le Roy C.I., Bell J.T., Spector T., Baumbach J., O'toole P.W., Peters A., and Haller D.* (2020). Arrhythmic Gut Microbiome Signatures Predict Risk of Type 2 Diabetes. Cell Host and Microbe 28, 258-272.

8. Metwaly A., Dunkel A., Waldschmitt N., Raj A.C.D., Lagkouvardos I., Corraliza A.M., Mayorgas A., Martinez-Medina M., Reiter S., Schloter M., Hofmann T., Allez M., Panes J., Salas A., and Haller D.* (2020). Integrated microbiota and metabolite profiles link Crohn’s disease to sulfur metabolism. Nature Communications 11, 4322. 

9. Khaloian S., Rath E., Hammoudi N., Gleisinger E., Blutke A., Giesbertz P., Berger E., Metwaly A., Waldschmitt N., Allez M., and Haller D.* (2020). Mitochondrial impairment drives intestinal stem cell transition into dysfunctional Paneth cells predicting Crohn's disease recurrence. Gut 69, 1939-1951.  

10. Coleman O.I., Lobner E.M., Bierwirth S., Sorbie A., Waldschmitt N., Rath E., Berger E., Lagkouvardos I., Clavel T., Mccoy K.D., Weber A., Heikenwalder M., Janssen K.P., and Haller D.* (2018). Activated ATF6 Induces Intestinal Dysbiosis and Innate Immune Response to Promote Colorectal Tumorigenesis. Gastroenterology 155, 1539-1552.

11. Rath E., Moschetta A., and Haller D.* (2018). Mitochondrial function — gatekeeper of intestinal epithelial cell homeostasis. Nature Reviews Gastroenterology and Hepatology 15, 497-516.

12. Yuan D., Huang S., Berger E., Liu L., Gross N., Heinzmann F., Ringelhan M., Connor T.O., Stadler M., Meister M., Weber J., Öllinger R., Simonavicius N., Reisinger F., Hartmann D., Meyer R., Reich M., Seehawer M., Leone V., Höchst B., Wohlleber D., Jörs S., Prinz M., Spalding D., Protzer U., Luedde T., Terracciano L., Matter M., Longerich T., Knolle P., Ried T., Keitel V., Geisler F., Unger K., Cinnamon E., Pikarsky E., Hüser N., Davis R.J., Tschaharganeh D.F., Rad R., Weber A., Zender L., Haller D.*, and Heikenwalder M.* (2017). Kupffer Cell-Derived Tnf Triggers Cholangiocellular Tumorigenesis through JNK due to Chronic Mitochondrial Dysfunction and ROS. Cancer Cell 31, 771-789.

13. Schaubeck M., Clavel T., Calasan J., Lagkouvardos I., Haange S.B., Jehmlich N., Basic M., Dupont A., Hornef M., Von Bergen M., Bleich A., and Haller D.* (2016). Dysbiotic gut microbiota causes transmissible Crohn's disease-like ileitis independent of failure in antimicrobial defence. Gut 65, 225-237. 

14. Berger E., Rath E., Yuan D., Waldschmitt N., Khaloian S., Allgäuer M., Staszewski O., Lobner E.M., Schöttl T., Giesbertz P., Coleman O.I., Prinz M., Weber A., Gerhard M., Klingenspor M., Janssen K.P., Heikenwalder M., and Haller D.* (2016). Mitochondrial function controls intestinal epithelial stemness and proliferation. Nature Communications 7, 13171. 

15. Von Schillde M.A., Hörmannsperger G., Weiher M., Alpert C.A., Hahne H., Bäuerl C., Van Huynegem K., Steidler L., Hrncir T., Pérez-Martínez G., Kuster B., and Haller D.* (2012). Lactocepin secreted by Lactobacillus exerts anti-inflammatory effects by selectively degrading proinflammatory chemokines. Cell Host and Microbe 11, 387-396.