I have a background in the execution of molecular biology research as a former laboratory technician for 5 years during and following my undergraduate degree in molecular, cellular, and developmental biology. I also have a background in epidemiology and statistics through my MPH at UC Berkeley during which time I mastered the application of meta-analysis and systematic review techniques to infectious diseases topics, in particular in my masters thesis on HIV directly observed therapy. In addition, my years at Stanford as an internal medicine resident, infectious diseases fellow, and immunocompromised infectious diseases fellow have further developed my desire to address important translational questions that will improve the clinical outcomes of the patients that I care for on the stem cell transplant service. I hope to find therapies that might safely and effectively supplement and even take the place of antibiotics for prophylaxis and treatment of GVHD and infectious complications.
Honors & Awards
American Society for Blood and Marrow Transplant New Investigator Award, ASBMT (2017-2019)
Dean's Postdoctoral Fellowship Award, Stanford (2017)
Boards, Advisory Committees, Professional Organizations
Member, Infectious Diseases Society of America (2013 - Present)
Member, American Society of Hematology (2015 - Present)
Member, American Society for Bone and Marrow Transplantation (2015 - Present)
MPH, University of California Berkeley, Epidemiology (2008)
Bachelor of Arts, University of California Santa Cruz, UG Other not listed (2002)
Doctor of Medicine, Stanford University, MED-MD (2010)
- The Microbiome and Hematopoietic Cell Transplantation: Past, Present, and Future. Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation 2018
- Antibiotics in Hematopoietic Cell Transplantation: Adversaries or Allies? BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION 2016; 22 (6): 972-974
Microbiota Manipulation With Prebiotics and Probiotics in Patients Undergoing Stem Cell Transplantation
CURRENT HEMATOLOGIC MALIGNANCY REPORTS
2016; 11 (1): 19-28
Hematopoietic stem cell transplantation (HSCT) is a potentially life-saving therapy that often comes at the cost of complications such as graft-versus-host disease and post-transplant infections. With improved technology to understand the ecosystem of microorganisms (viruses, bacteria, fungi, and microeukaryotes) that make up the gut microbiota, there is increasing evidence of the microbiota's contribution to the development of post-transplant complications. Antibiotics have traditionally been the mainstay of microbiota-altering therapies available to physicians. Recently, interest is increasing in the use of prebiotics and probiotics to support the development and sustainability of a healthier microbiota. In this review, we will describe the evidence for the use of prebiotics and probiotics in combating microbiota dysbiosis and explore the ways in which they may be used in future research to potentially improve clinical outcomes and decrease rates of graft-versus-host disease (GVHD) and post-transplant infection.
View details for DOI 10.1007/s11899-016-0302-9
View details for Web of Science ID 000372595100004
The Helicobacter pylori CZB cytoplasmic chemoreceptor TlpD forms an autonomous polar chemotaxis signaling complex that mediates a tactic response to oxidative stress.
Journal of bacteriology
Cytoplasmic chemoreceptors are widespread among prokaryotes but are far less understood than transmembrane chemoreceptors, despite being implicated in many processes. One such cytoplasmic chemoreceptor is Helicobacter pylori TlpD, which is required for stomach colonization and drives a chemotaxis response to cellular energy levels. Neither the signals sensed by TlpD nor its molecular mechanisms of action are known. We report that TlpD functions independently of the other chemoreceptors. When TlpD is the sole chemoreceptor, it is able to localize to the pole, and recruits CheW, CheA, and at least two CheV proteins to this location. It loses normal membrane association that appears to be driven by interactions with other chemoreceptors as well as CheW, CheV1, and CheA. These results suggest that TlpD can form an autonomous signaling unit. We further determined that TlpD mediates a repellent chemotaxis response to conditions that promote oxidative stress including iron, hydrogen peroxide, paraquat, and metronidazole. Lastly, we find that all tested H. pylori strains express TlpD, whereas other chemoreceptors are variably present. Our data suggest a model in which TlpD coordinates a signaling complex that responds to oxidative stress and may allow H. pylori to avoid stomach areas with high concentrations of reactive oxygen species.Helicobacter pylori senses its environment with proteins called chemoreceptors. Chemoreceptors integrate this sensory information to affect flagellar-based motility, in a process called chemotaxis. Chemotaxis is employed during infection and presumably aids H. pylori in encountering and colonizing preferred niches. A cytoplasmic chemoreceptor named TlpD is particularly important in this process and we report here that this chemoreceptor is able operate independently of other chemoreceptors to organize a chemotaxis signaling complex and mediate a repellent response to oxidative stress conditions. H. pylori encounters and must cope with oxidative stress during infection due to oxygen and reactive oxygen produced by host cells. TlpD's repellent response may allow the bacteria to escape niches experiencing inflammation and elevated ROS production.
View details for DOI 10.1128/JB.00071-16
View details for PubMedID 27002127
A supplemented soft agar chemotaxis assay demonstrates the Helicobacter pylori chemotactic response to zinc and nickel
2013; 159: 46-57
Directed motility, or chemotaxis, is required for Helicobacter pylori to establish infection in the stomach, although the full repertoire of this bacterium's chemotactic responses is not yet known. Here we report that H. pylori responds to zinc as an attractant and nickel as a repellent. To reach this conclusion, we employed both a temporal chemotaxis assay based on bacterial reversals and a supplemented soft agar spatial assay. We refined the temporal assay using a previously described chemorepellent, acid, and found that H. pylori requires rich media with serum to maintain optimal swimming motility. Surprisingly, we found that some strains respond to acid as an attractant, and that the TlpC chemoreceptor correlated with whether acid was sensed as an attractant or repellent. Using this same assay, we detected weak repellent responses to nickel and copper, and a varied response to zinc. We thus developed an alternative spatial chemotactic assay called the supplemented soft agar assay, which utilizes soft agar medium supplemented with the test compound. With Escherichia coli, the attractant serine slowed overall bacterial migration, while the repellent nickel increased the speed of overall migration. In H. pylori we detected slowed migration with doubled tryptone media, as well as zinc, consistent with an attractant response. In contrast, nickel increased migration, consistent with repulsion.
View details for DOI 10.1099/mic.0.062877-0
View details for Web of Science ID 000315561000005
View details for PubMedID 23139399
Helicobacter pylori chemotaxis modulates inflammation and bacterium-gastric epithelium interactions in infected mice
INFECTION AND IMMUNITY
2007; 75 (8): 3747-3757
The ulcer-causing pathogen Helicobacter pylori uses directed motility, or chemotaxis, to both colonize the stomach and promote disease development. Previous work showed that mutants lacking the TlpB chemoreceptor, one of the receptors predicted to drive chemotaxis, led to less inflammation in the gerbil stomach than did the wild type. Here we expanded these findings and examined the effects on inflammation of completely nonchemotactic mutants and mutants lacking each chemoreceptor. Of note, all mutants colonized mice to the same levels as did wild-type H. pylori. Infection by completely nonchemotactic mutants (cheW or cheY) resulted in significantly less inflammation after both 3 and 6 months of infection. Mutants lacking either the TlpA or TlpB H. pylori chemotaxis receptors also had alterations in inflammation severity, while mutants lacking either of the other two chemoreceptors (TlpC and HylB) behaved like the wild type. Fully nonchemotactic and chemoreceptor mutants adhered to cultured gastric epithelial cells and caused cellular release of the chemokine interleukin-8 in vitro similar to the release caused by the wild type. The situation appeared to be different in the stomach. Using silver-stained histological sections, we found that nonchemotactic cheY or cheW mutants were less likely than the wild type to be intimately associated with the cells of the gastric mucosa, although there was not a strict correlation between intimate association and inflammation. Because others have shown that in vivo adherence promotes inflammation, we propose a model in which H. pylori uses chemotaxis to guide it to a productive interaction with the stomach epithelium.
View details for DOI 10.1128/IAI.00082-07
View details for Web of Science ID 000248355200009
View details for PubMedID 17517875
Two predicted chemoreceptors of Helicobacter pylori promote stomach infection
INFECTION AND IMMUNITY
2002; 70 (10): 5877-5881
Helicobacter pylori must be motile or display chemotaxis to be able to fully infect mammals, but it is not known how this chemotaxis is directed. We disrupted two genes encoding predicted chemoreceptors, tlpA and tlpC. H. pylori mutants lacking either of these genes are fully motile and chemotactic in vitro and are as able as the wild type to infect mice when they are the sole infecting strains. In contrast, when mice are coinfected with the H. pylori SS1 tlpA or tlpC mutant and the wild type, we find more wild type than mutant after 2 weeks of colonization. Neither strain has an in vitro growth defect. These results suggest that the tlpA- and tlpC-encoded proteins assist colonization of the stomach environment.
View details for DOI 10.1128/IAI.70.10.5877-5881.2002
View details for Web of Science ID 000178125500066
View details for PubMedID 12228322