School of Medicine
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Maya Adam
Clinical Associate Professor, Pediatrics - Infectious Diseases
BioDr. Adam is the Director of Health Media Innovation and a Clinical Associate Professor in the Department of Pediatrics at Stanford School of Medicine. Her research focuses on measuring the impact of innovative, video-based entertainment-education approaches to global health communication. She produces short, animated films and online courses on topics related to maternal child health, nutrition, mental health and disease prevention. She has designed and produced online educational content for the Stanford School of Medicine for use in their preclinical programs, continuing medical education programs and global health promotion efforts. She is the Faculty Lead for the Global Child Health Media Initiative and Associate Director of the Center for Digital Health at Stanford. She is also the lead instructor of eight massive open online courses reaching more than a million learners around the world. Adam is principal investigator on two randomized-controlled trials investigating the impact of digital global health education interventions on health-promoting behaviors. Her research is conducted in collaboration with the Heidelberg Institute of Global Health in Heidelberg, Germany. She is a Faculty Fellow at the Center for Innovation in Global Health and the author of Food, Love, Family: A Practical Guide to Child Nutrition.
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Manuel R. Amieva
Professor of Pediatrics (Infectious Diseases) and of Microbiology and Immunology
Current Research and Scholarly InterestsMy laboratory studies how bacteria colonize our bodies for long periods of time, and how interactions between bacteria and the epithelial surfaces of the gastrointestinal tract and skin may lead to disease. Epithelial surfaces are the first barrier against infection, but they also where our bodies meet and co-evolve with the microbial world.. Several of our studies have focused on the epithelial junctions as a target for bacterial pathogens. The host epithelium uses its epithelial junctions to form a tight but dynamic barrier with an external surface that is inhospitable to microbial attachment, secretes anti-microbial compounds, and has a rapid rate of self-renewal. The balance in the microbe-epithelial relationship results in silent commensalism or symbiosis; an imbalance results in diseases ranging from acute bacterial invasive disease to chronic ulcers or carcinoma.
Our laboratory has developed novel microscopy applications such as quantitative 3D confocal microscopy, electron microscopy, time-lapse imaging, microinjection and micromanipulation to visualize the interaction of pathogens with epithelial cells in culture and in animal and human tissues. Many of out studies focus on the gastric pathogen Helicobacter pylori, but we have also expanded our investigations to include the intestinal pathogens Listeria monocytogenes and Salmonella enterica, and the skin pathogen and colonizer Staphylococcus aureus. I believe that elucidating how microbes communicate with and alter our epithelial cells at a molecular level will be important for finding novel therapeutic targets to control mucosal colonization and prevent invasive disease.
Using this perspective, we have uncovered several novel concepts of how bacteria colonize and breach our epithelial surfaces. For example, we discovered that Helicobacter pylori target the intercellular junctions, and in particular that the virulence factor CagA affects junction assembly and cell polarity. This confers H. pylori the ability to extract nutrients and grow directly on the epithelial surface. We also found that these properties of CagA have consequences for cellular transformation of the epithelium. For instance, we showed that H. pylori affect the activity and state of epithelial stem cells in the stomach by colonizing the epithelial surface deep in the gastric glands. This gland-associated population is essential for pathological inflammation and hyperplasia in animal models, and confers significant colonization advantages to the bacteria. Our Listeria research uncovered a new mechanism and site where bacteria can breach the gastrointestinal epithelial barrier to invade. We found that Listeria find their receptor for invasion at sites of epithelial senescence, where the epithelial junctions undergo dynamic turnover. To study Salmonella and H. pylori we have developed a human organoid model to study their interactions with human gut epithelium in vitro. To study Staphylococcus aureus pathogenesis, we have developed methods to visualize infection at the scale of a single bacterial microcolony using an organoid culture system of human keratinocytes and fibroblasts that grow into a 3D skin-equivalent. We recently identified several proteins at the eptithelial junctions as host factors involved in the pathogenesis of one of Staphylococcus aureus major toxins. -
Ann M. Arvin
Lucile Salter Packard Professor of Pediatrics and Professor of Microbiology and Immunology, Emerita
Current Research and Scholarly InterestsOur laboratory investigates the pathogenesis of varicella zoster virus (VZV) infection, focusing on the functional roles of particular viral gene products in pathogenesis and virus-cell interactions in differentiated human cells in humans and in Scid-hu mouse models of VZV cell tropisms in vivo, and the immunobiology of VZV infections.
