Bio

Dr. Maayan Levy received her Ph.D. in Immunology from the Weizmann Institute of Science. After completion of her PhD, Dr. Levy became an Assistant Professor at the Microbiology Department of the Perelman School of Medicine at the University of Pennsylvania. Dr. Levy has recently joined the Stanford Medicine Department of Pathology as an Assistant Professor and the Arc Institute as an Innovation Investigator in Residence.

Dr. Maayan Levy’s scientific mission is to understand, develop, and apply the concept of metabotherapy—the use of metabolites as vehicles and targets to prevent and treat disease. Her lab’s primary focus is on inflammatory diseases, neurological diseases, and cancer. Maayan is particularly interested in the metabolite landscape of the gastrointestinal tract, which serves as a major metabolite source for many other tissues and as an ideal entry point for the introduction of new metabolites into the organism. She is exploring the repertoire of these intestinal metabolites, their impact on whole-body physiology, and the possibility of targeting them for therapeutic interventions.

Among the recognitions that Dr. Levy’s work has received are the NIH Director’s New Innovator Award, Pew Biomedical Scholar Award, Searle Scholar Award, and Burroughs Wellcome Fund Investigator in the Pathogenesis of Infectious Disease Award.

Academic Appointments

Administrative Appointments

  • Innovation Investigator, Arc Institute (2025 - Present)

Contact

  • Academic
    levym@stanford.edu
    University - Faculty Department: Pathology Position: Asst Professor

Additional Info

  • Mail Code: 5324

Links

Current Research and Scholarly Interests

The Levy Lab at Stanford Pathology and the Arc Institute investigates how the microbiome communicates with the brain to regulate metabolism, behavior, and overall health. Their research focuses on uncovering how microbial signals influence neural circuits that control hunger, energy balance, and decision-making. By exploring these pathways, the lab aims to understand how disruptions in microbiome-brain communication contribute to diseases like obesity, diabetes, and psychiatric disorders.

A central goal of the Levy Lab is to identify the molecular mechanisms linking microbiome imbalances to disease states. By using cutting-edge tools such as optogenetics, imaging, and circuit mapping, they map how microbial metabolites and immune signals affect brain function. These insights offer a clearer understanding of how gut dysbiosis can drive metabolic dysfunction and mental health disorders.

The lab also investigates how restoring healthy microbiome-brain communication can reverse disease processes. By identifying key neural circuits and microbial pathways involved in disease, they work toward developing microbiome-targeted therapies. Potential applications include personalized treatments for obesity, metabolic syndrome, and anxiety or depression.

In addition, the Levy Lab emphasizes the importance of individual variability in microbiome composition. Their research explores how differences in microbial ecosystems may explain why some individuals are more susceptible to disease than others. This personalized approach informs the development of tailored therapies designed to restore health by targeting specific microbiome-related pathways.

Through its interdisciplinary approach, the Levy Lab provides valuable insights into the microbiome’s role in health and disease. Its discoveries offer promising avenues for innovative treatments and preventive strategies, paving the way for microbiome-based therapies that address a range of metabolic and neurological disorders.

2024-25 Courses

Stanford Advisees

All Publications

  • Microbial colonization programs are structured by breastfeeding and guide healthy respiratory development. Cell Shenhav, L., Fehr, K., Reyna, M. E., Petersen, C., Dai, D. L., Dai, R., Breton, V., Rossi, L., Smieja, M., Simons, E., Silverman, M. A., Levy, M., Bode, L., Field, C. J., Marshall, J. S., Moraes, T. J., Mandhane, P. J., Turvey, S. E., Subbarao, P., Surette, M. G., Azad, M. B. 2024; 187 (19): 5431-5452.e20

    Abstract

    Breastfeeding and microbial colonization during infancy occur within a critical time window for development, and both are thought to influence the risk of respiratory illness. However, the mechanisms underlying the protective effects of breastfeeding and the regulation of microbial colonization are poorly understood. Here, we profiled the nasal and gut microbiomes, breastfeeding characteristics, and maternal milk composition of 2,227 children from the CHILD Cohort Study. We identified robust colonization patterns that, together with milk components, predict preschool asthma and mediate the protective effects of breastfeeding. We found that early cessation of breastfeeding (before 3 months) leads to the premature acquisition of microbial species and functions, including Ruminococcus gnavus and tryptophan biosynthesis, which were previously linked to immune modulation and asthma. Conversely, longer exclusive breastfeeding supports a paced microbial development, protecting against asthma. These findings underscore the importance of extended breastfeeding for respiratory health and highlight potential microbial targets for intervention.

    View details for DOI 10.1016/j.cell.2024.07.022

    View details for PubMedID 39303691

    View details for PubMedCentralID PMC11531244

  • Serotonin reduction in post-acute sequelae of viral infection. Cell Wong, A. C., Devason, A. S., Umana, I. C., Cox, T. O., Dohnalová, L., Litichevskiy, L., Perla, J., Lundgren, P., Etwebi, Z., Izzo, L. T., Kim, J., Tetlak, M., Descamps, H. C., Park, S. L., Wisser, S., McKnight, A. D., Pardy, R. D., Kim, J., Blank, N., Patel, S., Thum, K., Mason, S., Beltra, J. C., Michieletto, M. F., Ngiow, S. F., Miller, B. M., Liou, M. J., Madhu, B., Dmitrieva-Posocco, O., Huber, A. S., Hewins, P., Petucci, C., Chu, C. P., Baraniecki-Zwil, G., Giron, L. B., Baxter, A. E., Greenplate, A. R., Kearns, C., Montone, K., Litzky, L. A., Feldman, M., Henao-Mejia, J., Striepen, B., Ramage, H., Jurado, K. A., Wellen, K. E., O'Doherty, U., Abdel-Mohsen, M., Landay, A. L., Keshavarzian, A., Henrich, T. J., Deeks, S. G., Peluso, M. J., Meyer, N. J., Wherry, E. J., Abramoff, B. A., Cherry, S., Thaiss, C. A., Levy, M. 2023; 186 (22): 4851-4867.e20

    Abstract

    Post-acute sequelae of COVID-19 (PASC, "Long COVID") pose a significant global health challenge. The pathophysiology is unknown, and no effective treatments have been found to date. Several hypotheses have been formulated to explain the etiology of PASC, including viral persistence, chronic inflammation, hypercoagulability, and autonomic dysfunction. Here, we propose a mechanism that links all four hypotheses in a single pathway and provides actionable insights for therapeutic interventions. We find that PASC are associated with serotonin reduction. Viral infection and type I interferon-driven inflammation reduce serotonin through three mechanisms: diminished intestinal absorption of the serotonin precursor tryptophan; platelet hyperactivation and thrombocytopenia, which impacts serotonin storage; and enhanced MAO-mediated serotonin turnover. Peripheral serotonin reduction, in turn, impedes the activity of the vagus nerve and thereby impairs hippocampal responses and memory. These findings provide a possible explanation for neurocognitive symptoms associated with viral persistence in Long COVID, which may extend to other post-viral syndromes.

    View details for DOI 10.1016/j.cell.2023.09.013

    View details for PubMedID 37848036

    View details for PubMedCentralID PMC11227373

  • The enteric nervous system relays psychological stress to intestinal inflammation. Cell Schneider, K. M., Blank, N., Alvarez, Y., Thum, K., Lundgren, P., Litichevskiy, L., Sleeman, M., Bahnsen, K., Kim, J., Kardo, S., Patel, S., Dohnalová, L., Uhr, G. T., Descamps, H. C., Kircher, S., McSween, A. M., Ardabili, A. R., Nemec, K. M., Jimenez, M. T., Glotfelty, L. G., Eisenberg, J. D., Furth, E. E., Henao-Mejia, J., Bennett, F. C., Pierik, M. J., Romberg-Camps, M., Mujagic, Z., Prinz, M., Schneider, C. V., Wherry, E. J., Bewtra, M., Heuckeroth, R. O., Levy, M., Thaiss, C. A. 2023; 186 (13): 2823-2838.e20

    Abstract

    Mental health profoundly impacts inflammatory responses in the body. This is particularly apparent in inflammatory bowel disease (IBD), in which psychological stress is associated with exacerbated disease flares. Here, we discover a critical role for the enteric nervous system (ENS) in mediating the aggravating effect of chronic stress on intestinal inflammation. We find that chronically elevated levels of glucocorticoids drive the generation of an inflammatory subset of enteric glia that promotes monocyte- and TNF-mediated inflammation via CSF1. Additionally, glucocorticoids cause transcriptional immaturity in enteric neurons, acetylcholine deficiency, and dysmotility via TGF-β2. We verify the connection between the psychological state, intestinal inflammation, and dysmotility in three cohorts of IBD patients. Together, these findings offer a mechanistic explanation for the impact of the brain on peripheral inflammation, define the ENS as a relay between psychological stress and gut inflammation, and suggest that stress management could serve as a valuable component of IBD care.

    View details for DOI 10.1016/j.cell.2023.05.001

    View details for PubMedID 37236193

    View details for PubMedCentralID PMC10330875

  • A microbiome-dependent gut-brain pathway regulates motivation for exercise. Nature Dohnalová, L., Lundgren, P., Carty, J. R., Goldstein, N., Wenski, S. L., Nanudorn, P., Thiengmag, S., Huang, K. P., Litichevskiy, L., Descamps, H. C., Chellappa, K., Glassman, A., Kessler, S., Kim, J., Cox, T. O., Dmitrieva-Posocco, O., Wong, A. C., Allman, E. L., Ghosh, S., Sharma, N., Sengupta, K., Cornes, B., Dean, N., Churchill, G. A., Khurana, T. S., Sellmyer, M. A., FitzGerald, G. A., Patterson, A. D., Baur, J. A., Alhadeff, A. L., Helfrich, E. J., Levy, M., Betley, J. N., Thaiss, C. A. 2022; 612 (7941): 739-747

    Abstract

    Exercise exerts a wide range of beneficial effects for healthy physiology1. However, the mechanisms regulating an individual's motivation to engage in physical activity remain incompletely understood. An important factor stimulating the engagement in both competitive and recreational exercise is the motivating pleasure derived from prolonged physical activity, which is triggered by exercise-induced neurochemical changes in the brain. Here, we report on the discovery of a gut-brain connection in mice that enhances exercise performance by augmenting dopamine signalling during physical activity. We find that microbiome-dependent production of endocannabinoid metabolites in the gut stimulates the activity of TRPV1-expressing sensory neurons and thereby elevates dopamine levels in the ventral striatum during exercise. Stimulation of this pathway improves running performance, whereas microbiome depletion, peripheral endocannabinoid receptor inhibition, ablation of spinal afferent neurons or dopamine blockade abrogate exercise capacity. These findings indicate that the rewarding properties of exercise are influenced by gut-derived interoceptive circuits and provide a microbiome-dependent explanation for interindividual variability in exercise performance. Our study also suggests that interoceptomimetic molecules that stimulate the transmission of gut-derived signals to the brain may enhance the motivation for exercise.

    View details for DOI 10.1038/s41586-022-05525-z

    View details for PubMedID 36517598

    View details for PubMedCentralID PMC11162758

  • β-Hydroxybutyrate suppresses colorectal cancer. Nature Dmitrieva-Posocco, O., Wong, A. C., Lundgren, P., Golos, A. M., Descamps, H. C., Dohnalová, L., Cramer, Z., Tian, Y., Yueh, B., Eskiocak, O., Egervari, G., Lan, Y., Liu, J., Fan, J., Kim, J., Madhu, B., Schneider, K. M., Khoziainova, S., Andreeva, N., Wang, Q., Li, N., Furth, E. E., Bailis, W., Kelsen, J. R., Hamilton, K. E., Kaestner, K. H., Berger, S. L., Epstein, J. A., Jain, R., Li, M., Beyaz, S., Lengner, C. J., Katona, B. W., Grivennikov, S. I., Thaiss, C. A., Levy, M. 2022; 605 (7908): 160-165

    Abstract

    Colorectal cancer (CRC) is among the most frequent forms of cancer, and new strategies for its prevention and therapy are urgently needed1. Here we identify a metabolite signalling pathway that provides actionable insights towards this goal. We perform a dietary screen in autochthonous animal models of CRC and find that ketogenic diets exhibit a strong tumour-inhibitory effect. These properties of ketogenic diets are recapitulated by the ketone body β-hydroxybutyrate (BHB), which reduces the proliferation of colonic crypt cells and potently suppresses intestinal tumour growth. We find that BHB acts through the surface receptor Hcar2 and induces the transcriptional regulator Hopx, thereby altering gene expression and inhibiting cell proliferation. Cancer organoid assays and single-cell RNA sequencing of biopsies from patients with CRC provide evidence that elevated BHB levels and active HOPX are associated with reduced intestinal epithelial proliferation in humans. This study thus identifies a BHB-triggered pathway regulating intestinal tumorigenesis and indicates that oral or systemic interventions with a single metabolite may complement current prevention and treatment strategies for CRC.

    View details for DOI 10.1038/s41586-022-04649-6

    View details for PubMedID 35477756

    View details for PubMedCentralID PMC9448510