Marlies Meisel, Ph.D.

Marlies Meisel, Ph.D.


Campus: The Assembly, 5051 Centre Ave

Office: 3041

Pittsburgh, PA 15213

Ph: 312-513-2106

Website »


  • University of Chicago, USA – Postdoc (2013-2018)
  • Medical University Innsbruck, Austria - Ph.D. (2012)
  • Nutritional Sciences at the University of Vienna, Austria - M.S. (2007)

Academic Affiliation

  • Assistant Professor, Department of Immunology

About Research

How does the gut microbiota shape systemic immunity?

Our lab is striving to define how the commensal gut microbiota, environmental/metabolic factors and the genetic/epigenetic equipment of the host impacts on systemic immunity during health and complex diseases, such as multiple sclerosis (MS), inflammatory bowel disease (IBD), Alzheimer’s disease liver fibrosis/hepatocellular carcinoma and cancer.



One of the main goals in our lab is to define the mechanism how commensal gut microbial signals initiate pre-cancerogenic liver fibrosis.

Hepatic fibrosis is the result of chronic liver damage from various etiologies including alcohol abuse, obesity, viral hepatitis or is of idiopathic origin and affects several million people in the United States. In general, LF is reversible, however chronic fibrotic liver disease may progress to cirrhosis and/or hepatocellular cancer (eventually requiring a liver transplant) that are irreversible end stage diseases. Despite the fact that hepatic fibrosis is a major health concern, and microbial signals correlate with disease severity, so far there are no direct cause-effect studies that mechanistically demonstrate the impact of systemic microbial signals on the development of LF. 

Sophisticated in vivo transgenic mice, gnotobiotic mice, fecal microbial transplants (mouse/humans)) and in vitro approaches are combined with single cell RNAseq as well as Next Gen metagenomic sequencing.  In this project our lab collaborates with the Liver Research Center in Pittsburgh to establish a strong translational axis. 

The ultimate goal is to identify novel biomarkers of early onset fibrosis, which help to identify individuals at risk to develop primary liver fibrosis and to develop novel treatment options to prevent/revert fibrosis and thus avoid liver cancer.



It is known that bacteria inhabit the tumor microenvironment. However there are several fundamental questions that have not been addressed in sufficient detail.
Do some bacteria inhabit only specific tumors (tissue specificity)?
Can bacteria impact cancer immune therapy via modulating the host immune system?
How do tumor intrinsic bacteria modulate the tumor microenvironment?
Besides tumor mouse models, this project will have a strong translational link by collaborating with the transplant center and the liver research center in Pittsburgh.



Our lab aims to interrogate how microbial signals affect the immune system of the host. In particular, we want to study how hematopoietic stem cells (HSCs) are affected by microbial signals in health and during disease in the context of trained immunity. The field of trained immunity is understudied. It is very intriguing that both murine and human HSC’s express TLRs, such as TLR2, TLR4 and TLR9 and thus are evolutionary prone to directly respond to microbial signals. Even more, microbial signals have the capacity to alter the transcriptional program and are able to dictate the differentiation of HSCs into either the myeloid or lymphoid linage. Furthermore, bacterial stimuli can train HSCs and their progenitors, which result in mature progeny that is equipped with a different transcriptional profile that enables them to better respond to a re-occurring bacterial stimulus. We will address the scientific questions by usage of several transgenic mouse lines, single cell RNAseq of sorted cell populations combined with in vitro and imaging tools. We will collaborate with several clinical institutions @ Pittsburgh to address human relevance of the study.



The host is constantly communicating with microbes. The human body is not sterile and live bacteria can be detected in healthy individuals. What leads to gut bacterial translocation? And is there a specific “window of opportunity” where gut microbiota predominately translocates into extra-intestinal organs?
Germ free mice are much more susceptible to infections and have a substantially impaired myeloid immune system. Is there a requirement for bacterial translocation? Is this a symbiotic process, which is beneficial to the host? Is this a required mechanism that trains the innate immune system to combat infections? 
Our lab will define which microbial (type/strain of commensal), environmental/metabolic (age, nutritional status, temperature) and genetic/epigenetic factors impact on spontaneous gut bacterial translocation and will evaluate its effects on development of the immune system during health and distress. 
We will use a strong imaging approach, bacterial flow cytometry/sorting, genetic bacterial engineering and gnotobiotic mouse models combined with targeted fecal microbial transplants and metagenomic/metatranscriptomic sequencing.


The Meisel lab is currently accepting graduate students for rotations in the laboratory, as well as applications for postdoctoral fellows.

Selected Publications

Meisel M#, Hinterleitner R#, Pacis A, Buscarlet M, Chen L, Pierre J, Bouziat R, Ernest J, Ringus D, Galipeau H, Armstrong S, McDonald B, Zurenski M, Musch M, Furtado G, Lira S, Chang E, E. Verdu, Godley L, Busque L, Barreiro L and Jabri B. Microbial signals drive Tet2-mediated pre-leukemic myeloproliferation. NATURE, 2018 May;557(7706):580-584. # contributed equally

Caminero A#, McCarville J#, Galipeau H#, Deraison C, Bernier S, Meisel M, Murray J, Yu B, Alaedini A, Coombes B, Sanz Y, Ruf W, Jabri B, Casqueiro J, Surette M, Vergnolle N and Verdu E. Microbial proteases increase sensitivity to dietary antigen through PAR-2; submitted to Nature communications; # contributed equally

Meisel M#, Caminero A#, Jabri B, and Verdu E. Mechanisms by which enteric microbes gear food sensitivities. Nature Reviews Gastroenterology & Hepatology, accepted March 2018; # contributed equally

Bunker J, Erickson S, Flynn T, Henry-Dunand C, Koval J, Meisel M, Jabri B, Antonopoulos D, Wilson P, and Bendelac A. Natural polyreactive IgA antibodies coat the intestinal microbiota. SCIENCE, 2017 Oct 20; 358(6361)

Minter MR, Meisel M#, Hinterleitner#, Zhang C#, Leone V, Zhang X, Oyler-Castrillo P, Musch MW, Jabri B, Chang EB, Tanzi RE, Sisodia SS. Antibiotic-induced perturbations in microbial diversity during development alters amyloid pathology in APPSWE/PS1ΔE9 murine model of Alzheimer’s disease. SCIENTIFIC REPORTS, 2017 Sept 5; 7(1):10411; # contributed equally

Bouziat R#, Hinterleitner R#, Brown JJ#, Stencel-Baerenwald JE, Ikizler M, Mayassi T, Meisel M, Kim SM, Discepolo V, Pruijssers AJ, Ernest JD, Iskarpatyoti JA, Costes LMM, Lawrence I, Palanski BA, Varma M, Zurenski MA, Khomandiak S, McAllister N, Aravamudhan P, Boehme KW, Hu F, Samsom JN, Reinecker HC, Kupfer SS, Guandalini S, Semrad C, Abadie V, Khosla C, Barreiro LB, Xavier RJ, Ng A, Dermody TS, Jabri B. Reovirus infection breaks tolerance to dietary antigens and promotes development of celiac disease. SCIENCE, 2017 Apr 7; 356(6333):44-50. # contributed equally

Meisel M, Mayassi T, Fehlner-Peach H, Koval JC, O’Brien SA, Hinterleitner R, Lesko K, Kim S, Bouziat R, Chen L, Weber CR, Mazmanian SK, Jabri B# and Antonopoulos DA#. Interleukin-15 promotes intestinal dysbiosis with butyrate deficiency associated with increased susceptibility to colitis. International Society for Microbial Ecology Journal; ISME J 2017 Jan;11(1):15-30

Galipeau H*, McCarville JL*, Huebener S, Litwin O, Meisel M, Jabri B, Murray JA, Jordana M, Alaedini A, Chirdo FG, Verdu EF. Intestinal microbiota modulates gluten-induced immunopathology in humanized mice. The American Journal of Pathology 2015 Nov; 185 (11):2970-2982 * contributed equally

Bunker JJ, Flynn TM, Koval JC, Shaw DG, Meisel M, McDonald BD, Ishizuka IE, Dent AL, Wilson PC, Jabri B, Antonopoulos DA, and Bendelac A. Innate and Adaptive Humoral Responses Coat Distinct Commensal Bacteria with Immunoglobulin A. IMMUNITY 2015 Sept 15; 43(1):1-13

Meisel M, Hermann-Kleiter N, Hinterleitner R, Gruber T, Pfeifhofer-Obermair C, Wachowicz K, Viola A, Soldani C, Fresser F, Leitges M, Kaminski S, Baier G. The kinase PKC selectively upregulates interleukin-17A during Th17 cell immune responses. IMMUNITY. 2013 Jan 24;38(1):41-52


Complete list of publications