About

Liz Johnson, PhD, is an Associate Professor and Principal Investigator at the Johnson Lab. She is a molecular biologist specializing in genomic and metabolomic approaches to studying the effects of nutrition on the gut microbiome. She completed her postdoctoral training in the lab of Ruth Ley at the Department of Microbiome Science, Max Planck Institute for Developmental Biology in Tübingen, Germany, and collaborated with the lab of Tilla Worgall at the Institute of Human Nutrition, Columbia University, New York, NY. She earned her PhD in Molecular Biology from Princeton University, where she used high-throughput sequencing techniques to understand how cells maintain cellular integrity during times of prolonged cell cycle arrest.

Research topics

• Biology
• Genetics
• Computer Science
• Medicine
• Sociology
• Biochemistry
• Endocrinology
• Environmental health
• Microbiology
• Physiology
• Immunology
• Bioinformatics
• Internal medicine
• Obstetrics
• Cell biology
• Data science
• Ecology

Selected publications

• The potential importance of the built-environment microbiome and its impact on human health

  Proceedings of the National Academy of Sciences · 2024 · 45 citations

  • Computer Science
  • Sociology
  • Biology

  There is increasing evidence that interactions between microbes and their hosts not only play a role in determining health and disease but also in emotions, thought, and behavior. Built environments greatly influence microbiome exposures because of their built-in highly specific microbiomes coproduced with myriad metaorganisms including humans, pets, plants, rodents, and insects. Seemingly static built structures host complex ecologies of microorganisms that are only starting to be mapped. These microbial ecologies of built environments are directly and interdependently affected by social, spatial, and technological norms. Advances in technology have made these organisms visible and forced the scientific community and architects to rethink gene-environment and microbe interactions respectively. Thus, built environment design must consider the microbiome, and research involving host-microbiome interaction must consider the built-environment. This paradigm shift becomes increasingly important as evidence grows that contemporary built environments are steadily reducing the microbial diversity essential for human health, well-being, and resilience while accelerating the symptoms of human chronic diseases including environmental allergies, and other more life-altering diseases. New models of design are required to balance maximizing exposure to microbial diversity while minimizing exposure to human-associated diseases. Sustained trans-disciplinary research across time (evolutionary, historical, and generational) and space (cultural and geographical) is needed to develop experimental design protocols that address multigenerational multispecies health and health equity in built environments.

  PublisherOA PDFDOI

• Gestational diabetes is driven by microbiota-induced inflammation months before diagnosis

  Gut · 2023 · 149 citations

  • Medicine
  • Obstetrics
  • Bioinformatics

  OBJECTIVE: Gestational diabetes mellitus (GDM) is a condition in which women without diabetes are diagnosed with glucose intolerance during pregnancy, typically in the second or third trimester. Early diagnosis, along with a better understanding of its pathophysiology during the first trimester of pregnancy, may be effective in reducing incidence and associated short-term and long-term morbidities. DESIGN: We comprehensively profiled the gut microbiome, metabolome, inflammatory cytokines, nutrition and clinical records of 394 women during the first trimester of pregnancy, before GDM diagnosis. We then built a model that can predict GDM onset weeks before it is typically diagnosed. Further, we demonstrated the role of the microbiome in disease using faecal microbiota transplant (FMT) of first trimester samples from pregnant women across three unique cohorts. RESULTS: We found elevated levels of proinflammatory cytokines in women who later developed GDM, decreased faecal short-chain fatty acids and altered microbiome. We next confirmed that differences in GDM-associated microbial composition during the first trimester drove inflammation and insulin resistance more than 10 weeks prior to GDM diagnosis using FMT experiments. Following these observations, we used a machine learning approach to predict GDM based on first trimester clinical, microbial and inflammatory markers with high accuracy. CONCLUSION: GDM onset can be identified in the first trimester of pregnancy, earlier than currently accepted. Furthermore, the gut microbiome appears to play a role in inflammation-induced GDM pathogenesis, with interleukin-6 as a potential contributor to pathogenesis. Potential GDM markers, including microbiota, can serve as targets for early diagnostics and therapeutic intervention leading to prevention.

  DOI

• Characterization of interactions of dietary cholesterol with the murine and human gut microbiome

  Nature Microbiology · 2022 · 121 citations

  Senior authorCorresponding
  • Biology
  • Biochemistry
  • Genetics

  Consumption of dietary lipids, such as cholesterol, modulates the gut microbiome with consequences for host health through the production of microbiome-derived metabolites. Despite the implications for host metabolism, a limited number of specific interactions of the gut microbiome with diet-derived lipids have been characterized. This is partially because obtaining species-level resolution of the responsible taxa can be challenging and additional approaches are needed to identify health-relevant metabolites produced from cholesterol-microbiome interactions. Here we performed bio-orthogonal labelling sort sequence spectrometry, a click chemistry based workflow, to profile cholesterol-specific host-microbe interactions. Mice were exposed to an alkyne-functionalized variant of cholesterol and 16S ribosomal RNA gene amplicon sequencing of faecal samples identified diet-derived cholesterol-interacting microbes from the genera Bacteroides, Bifidobacterium, Enterococcus and Parabacteroides. Shotgun metagenomic analysis provided species-level resolution of diet-derived cholesterol-interacting microbes with enrichment of bile acid-like and sulfotransferase-like activities. Using untargeted metabolomics, we identify that cholesterol is converted to cholesterol sulfate in a Bacteroides-specific manner via the enzyme BT_0416. Mice monocolonized with Bacteroides thetaiotaomicron lacking Bt_0416 showed altered host cholesterol and cholesterol sulfate compared with wild-type mice, identifying a previously uncharacterized microbiome-transformation of cholesterol and a mechanism for microbiome-dependent contributions to host phenotype. Moreover, identification of a cholesterol-responsive sulfotransferase in Bacteroides suggests diet-dependent mechanisms for altering microbiome-specific cholesterol metabolism. Overall, our work identifies numerous cholesterol-interacting microbes with implications for more precise microbiome-conscious regulation of host cholesterol homeostasis.

  DOI

• Sphingolipids produced by gut bacteria enter host metabolic pathways impacting ceramide levels

  Nature Communications · 2020 · 349 citations

  1st authorCorresponding
  • Biology
  • Microbiology
  • Cell biology

  Gut microbes are linked to host metabolism, but specific mechanisms remain to be uncovered. Ceramides, a type of sphingolipid (SL), have been implicated in the development of a range of metabolic disorders from insulin resistance (IR) to hepatic steatosis. SLs are obtained from the diet and generated by de novo synthesis in mammalian tissues. Another potential, but unexplored, source of mammalian SLs is production by Bacteroidetes, the dominant phylum of the gut microbiome. Genomes of Bacteroides spp. and their relatives encode serine palmitoyltransfease (SPT), allowing them to produce SLs. Here, we explore the contribution of SL-production by gut Bacteroides to host SL homeostasis. In human cell culture, bacterial SLs are processed by host SL-metabolic pathways. In mouse models, Bacteroides-derived lipids transfer to host epithelial tissue and the hepatic portal vein. Administration of B. thetaiotaomicron to mice, but not an SPT-deficient strain, reduces de novo SL production and increases liver ceramides. These results indicate that gut-derived bacterial SLs affect host lipid metabolism.

  DOI

Recent grants

• Lipid-dependent host-microbe interactions

  NIH · $2.6M · 2020–2030

Frequent coauthors

• Hilary A. Coller

  University of California, Los Angeles

  25 shared

• Min-Ting Lee

  Cornell University

  15 shared

• Ruth E. Ley

  Max Planck Institute for Biology

  14 shared

• Mithun Mitra

  University of California, Los Angeles

  14 shared

• Henry H. Le

  Fred Hutch Cancer Center

  13 shared

• Eran Elinav

  Weizmann Institute of Science

  12 shared

• Sven Pettersson

  National University of Singapore

  12 shared

• Aaron Ambrus

  University of California, Los Angeles

  12 shared

Education

• B.S., Biology

  Spelman College

• Ph.D., Cell cycle transcriptomics

  Princeton University

Awards & honors

• Howard Hughes Medical Institute Freeman Hrabowski Scholar

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