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NW Microbiome Network Hosts:
MICROBIOME MIXER
8:30 AM – 9:15 AM Arrival, check‐in, poster set‐up; breakfast available
9:15 AM – 10:00 AM Structured Networking; breakfast available
10:00 AM – 10:15 AM Welcome! Introductory Remarks
10:15 AM – 11:45 AM Individual Presentations Followed by Panel‐style Q & A
Can we use microbiomes to predict or diagnose host or environmental health? Moderator: Chris Gaulke Brendan Bohannan, PhD Thomas Sharpton, PhD Kim Brown, PhD Ryan McClure, PhD Justin Merritt, PhD 11:45 AM – 1:00 PM Lunch + Poster Session
1:00 PM – 2:30 PM Individual Presentations Followed by Panel‐style Q & A
Does the future of health care or ecological conservation involve microbiome management?
Moderator: Hannah Tavalire Natalia Shulzhenko, MD, PhD Anne Thompson, PhD Jon M. Jacobs, PhD Karen Guillemin, PhD Amy Moran, PhD 2:30 PM – 3:30 PM Overview: Institutional Resources
3:30 PM – 4:15 PM (^) Identifying Areas for Future Collaborations
4:15 PM – 4:30 PM
Looking Forward: Closing Remarks
Brendan Bohannan
Brendan Bohannan, Ph.D., is the Alec and Kay Keith Professor of Environmental Studies and Biology at the University of Oregon’s Institute of Ecology and Evolution. His research is focused on understanding the causes and consequences of microbial biodiversity. He began his research career studying microbes in non‐host environments (such as soil, water, air, and built environments), but over the past 12 years his group has increasingly focused on the microbiomes of humans and other animals (including fish, birds and primates). He is especially interested in how transmission (among hosts, and between hosts and the external environment) interacts with host factors (such as individual genetics and physiology) to determine the composition of host‐associated microbiomes. His group is also interested in how host‐microbe system‐level functions (such as digestion, or stimulation of the immune system) emerge from the complexity of host‐microbe interactions. Professor Bohannan is a founding member of the Microbial Ecology and Theory of Animals Center for Systems Biology (an NIH Center of Excellence focused on the application of ecological theory to host‐microbe systems) and the Biology and the Built Environment Center (a national center for the study of the microbial ecology of buildings). He is a Fellow of the American Academy of Microbiology, as well as an Aldo Leopold Environmental Leadership Fellow, a Google Science Communication Fellow, and a Wulf Professor of the Humanities. Prof. Bohannan received a Ph.D. in Microbiology from Michigan State University and post‐doctoral training in Ecology at the University of Chicago, before joining the Stanford University faculty in 1999. He has been a member of the University of Oregon faculty since 2006
Thomas Sharpton
Thomas Sharpton is an Assistant Professor at Oregon State University. He earned his Ph.D. in Microbiology from the University California at Berkeley in 2009 with a Designated Emphasis in Computational Biology. He subsequently received his postdoctoral training at the Gladstone Institutes in San Francisco, CA, wherein he pioneered computational tools and data resources to characterize the human metagenome. In 2013, he joined OSU as a faculty member in the Departments of Microbiology and Statistics. In addition to teaching students in the classroom, Dr. Sharpton runs an internationally recognized research laboratory that applies molecular, computational, and statistical methods to determine how the gut microbiome influences the health, ecology, and evolution of vertebrates. Dr. Sharpton also serves as the Founding Director of the Oregon State University Microbiome Initiative, which seeks to transform how we study and conceptualize microbiomes, disseminate microbiome‐related education and training, and expand the public’s involvement and interest in this exciting and rapidly growing research arena.
Kim Brown
I received my Ph.D. from Washington State University in 2004 and completed two post‐doctoral training positions. In my first post‐doc at the University of Idaho, I worked on the effects of environmental estrogens, specifically the major form of female birth control (17α‐ethynylestradiol), and their consequences on male rainbow trout reproductive physiology. From there I moved into cytogenetic research in my second fellowship at Harvard Medical School and Brigham and Women's Hospital in Boston, MA. This work focused on Copy Number Variants (CNVs) in the model organism zebrafish. Future work will combine these interests to look at whether environmental contaminants can alter genome structure.
Ryan McClure
Dr. Ryan McClure’s research is focused on using network analyses to understand interactions both within and between microbial species and between microbes and the host. His work mainly focuses on collecting large datasets of transcriptomic and other kinds of ‐omics data across conditions and environments to determine where there is coordination between species, genes, proteins and metabolites. This data can then be mined to better understanding which species may be particularly important to certain microbiomes and how species within microbiomes may interact. He has applied these approaches to microbiomes of soil and of the human host as well as to individual microbial species such as cyanobacteria and human pathogens. In addition, Dr. McClure has experience in synthetic biology and applies this to better understand and control interactions between microbial species, including those that may be predicted from network analysis.
Justin Merritt
Dr. Merritt’s research focuses on the mechanisms used by signal transduction systems to control various virulence properties of several bacterial pathogens associated with oral disease. Research in my laboratory is focused upon the genetic regulatory mechanisms linking the control of various accessory/virulence gene pathways with the sensing of environmental stress. We study members of the human oral flora as our model system for the role of microbial ecology in determining health and disease at mucosal sites in the human body. Our primary organism of interest is Streptococcus mutans, which is one of the principal species responsible for triggering tooth decay (dental caries) as result of dysbiosis among the oral flora. However, our research also often involves studies of a variety of other oral bacterial species, especially for studies of interspecies interactions among the oral flora. In addition, we have recently begun examining the role of Anginosus group streptococci in the formation of oral and systemic abscesses. Treatment of dysbiotic diseases caused by the flora, such as oral diseases, irritable bowel disease, vaginosis, etc. poses a unique challenge because the few species associated with pathology live amongst potentially hundreds of other beneficial species in mixed communities. Thus, the typical antibiotic treatment approaches used for many other types of infections are either ineffective or can result in serious side effects. Ultimately, effective solutions will require new ecological treatment strategies that reestablish symbiosis among the flora.
Kate Bowie BS Graduate Student
David Ellison MD Director/Assoc VP for Clinical & Translational Research Ruth Etzioni PhD Distinguished Scientist, CEDAR Jack Ferracane PhD Professor and Chair Ian Fields MD Fellow Physician Alex* Foster MD, MPH Assistant Professor
Mark Garzotto MD Professor of Urology an Radiation Medicine
JP Gourdine PhD Senior Research Associate
Britt* Gratreak BS Research Assistant II
Tom Gregory MD Professor, Urogynecology
Teri* Greiling MD, PhD Assistant Professor of Dermatology
Anna Hunter MD Assistant Professor of Pediatrics
Younes Jahangiri MD Postdoctoral Scholar
Jeni Johnstone PhD Faculty Researcher
Lisa Karstens PhD Assistant Professor
Jens* Kreth PhD Associate Professor Raj Kulkarni MD, PhD Assistant Professor Mike Lane MD Assistant Professor, Neurology
Eric Leung PhD Candidate PhD Candidate
David Lieberman MD Professor of Medicine, Chief Division of Gastroenterology Jen Lillemon MD Fellow
Daniel Marks MD, PhD Sr. Associate Dean for Research, Professor
Bob Martindale MD, PhD Chief Division of General and Gastrointestinal Surgery
Justin Merritt PhD Professor
Amy Moran PhD Assistant Professor
Cindy Morris PhD MPH Professor Yukiko Nakamura PhD Postdoc Researcher
Rahel Nardos MD, MCR Dr/ Assistant Professor
Courtney* Armour Graduate Research Assistant
Vrushali Bokil PhD Professor & Associate Head
Chris* Burgess Graduate Student
Jessica* Buser
PhD Student Graduate Student
Jeff Chang PhD Associate Professor
Rick Colwell PhD Professor
Claire* Couch BSc PhD Candidate Maude* David PhD Assistant Professor
Ed* Davis PhD Bioinformatics Analyst
Theo* Dreher PhD Professor
Emily Dziedzic MS Graduate Student
Charlotte Eriksson PhD student
PhD student
Xiaoli Fern PhD Associate Professor
Manuel Garcia‐ Jaramillo PhD Research Associate (Postdoc)
Chris Gaulke PhD Research Associate
Steve Giovannoni PhD Distinguished Professor
Fritz* Gombart PhD Professor of Biochemistry and Biophysics Manoj* Gurung PhD Graduate Research Assistant Keisha Rose* Harrison PhD Candidate Graduate Student
Emily* Ho PhD Professor and Director
Duo Jiang PhD Assistant Professor
Yuan Jiang PhD Associate Professor
Jared Johnson MS PhD Student Michael* Kent PhD Professor Grace* Klinges BS PhD Student, GRFP Fellow
Jung Kwon PhD Assistant Professor
Kelsey Lane
MS
student MS Graduate Student
Ryan* Mueller PhD Assoc. Professor Dave* Myrold PhD Professor
Sheryl* Bell Scientist
Stephen* Callister PhD Senior Research Scientist
Rob* Egbert PhD Senior Staff Scientist
Yuliya Farris BS Technician Whitney Garcia PhD intern Jon Jacobs PhD Senior Research Scientist
Young‐ Mo* Kim PhD Senior Scientist
Ryan* McClure PhD Scientist
Bill Nelson PhD Scientist
Karin Rodland PhD
Director, Precision Medicine Innovation Co‐ Laboratory
Mehmet Balkan MS Lab Manager/Research Scientist
Kim Brown PhD Assistant Professor
Brad Buckley PhD Associate Professor Brooke Napier PhD Assistant Professor Rahul Raghavan PhD Associate Professor Andrew Roberts UG Bio Student
Anne Thompson PhD Research Assistant Professor
Ste Traxler Undergraduate
From the Portland Community
Ryan Bradley ND, MPH Director of Research and Associate Professor
National University of Natural Medicine
Jenn* Ryan ND, MS Investigator National University of Natural Medicine
Alex Frye MSc Research Associate II
Providence; Earle A Chiles Research Institute
Annah Rolig PhD Research Scientist
Providence; Earle A Chiles Research Institute
Leslie Leve PhD Professor and Associate Vice President for Research
Beth* Miller PhD Postdoc
Nicolae Morar PhD Assistant Professor of Environmental Studies and Philosophy
Vanessa Ringgold MA, JD Licensing & Contracts Associate
Elinor Sullivan PhD Associate Professor
Hannah Tavalire MS, PhD Postdoctoral Research Scholar
Nelson Ting PhD Associate Professor
Doug Turnbull PhD Director, Genomics and Cell Characterization Core Facility
Poster Abstracts
A Metagenomic Meta‐Analysis Reveals Functional Signatures of Health and Disease in the Human Gut Microbiome Presented at 2018 Lake Arrowhead Microbial Genomics Conference Courtney Armour
Oregon State University
While recent research indicates that human health depends, in part, upon the symbiotic relationship between gut microbes and their host, the specific interactions between a host and its microbiome that define health remain poorly resolved. Metagenomic clinical studies can reveal gut microbial functions that stratify healthy and diseased individuals. However, the typical single‐disease focus of microbiome studies limits insight into which microbiome features robustly associate with health, indicate general deviations from health, or predict specific diseases. To improve our understanding of the association between the gut microbiome and health, we conducted the first integrative functional analysis of gut metagenomes by collecting all available clinical metagenomic data, which consists of about 2, samples obtained from eight clinical studies. Using a regression modeling approach, we robustly resolve functions in the microbiome that stratify diseased individuals from controls, and when possible control for study‐specific effects. Functions that indicate multiple diseases occur at a greater rate than expected by chance, which bolsters the likelihood that these functions contribute to health. We also resolve indicator functions of specific diseases, which point to disease‐specific etiologies. Many of these disease indicators also overlap with functions that stratify vertebrate microbiomes relative to free‐living microbial communities, further supporting their potential importance to host health. Overall, these results clarify potential microbiome‐mediated mechanisms of disease and reveal features of the microbiome that may be useful for the development of microbiome‐based diagnostics. Autoinducer‐2 Mediates Growth Mode of Bacterial Communities in the Zebrafish Intestine Maria Banuelos
University of Oregon
The vertebrate gut is home to a large and diverse microbiota that plays important roles in host health. As we learn more about these microbial communities we are beginning to understand that the spatial organization of these bacterial communities and their growth mode (i.e. planktonic vs aggregated) influence their interactions with one another and the host. However the mechanisms governing spatial organization and growth patterns in vivo are not well understood. Here we investigate the role of bacterial interspecies quorum sensing signal Autoinducer‐2 (AI‐2) in determining the growth mode and spatial patterning of bacterial communities in vivo. To address this we colonized larval zebrafish with wild type E.coli, AI‐2 synthesis mutant ∆luxS, or AI‐2 signaling mutant ∆lsrR. We used light sheet fluorescence microscopy to observe the growth mode and localization of the populations in vivo and measure intestinal abundance of the bacteria. We observe that wild type E.coli are found in large aggregate populations with few planktonic cells while ∆luxS consists of many small aggregates and with more planktonic cells. Consistent with previous work from our lab showing that largely aggregated bacterial communities are susceptible to expulsion from the gut, we found the aggregated wild type populaƟons at lower abundance than the more planktonic ∆luxS and ∆lsrR mutants. We also observe differing spaƟal localizaƟons between wild type and ∆luxS, with the wild type localized more distally along the axis of the intestine, consistent with increased displacement. Lastly, we were able to alter abundance levels of wild type by co‐colonizing with strains that change AI‐2 concentration in the intestine. This study offers evidence that AI‐ signaling is an important factor in growth mode and spatial organization of bacterial communities in the vertebrate gut that could be used for microbiota engineering.
Molecular composition of field derived microbial necromass Presented at 2019 Genomic Sciences Program Annual Principal Investigator (PI) Meeting Sheryl Bell
Pacific Northwest National Laboratory
Crop selection and soil texture influence the physicochemical attributes of the soil, which structures microbial communities and influences soil organic matter formation, cycling and long‐term storage. At the molecular scale, microbial metabolites and necromass alter the soil environment, which creates feedbacks that influence ecosystem functions, including soil organic matter accumulation. Yet the generalizable mechanisms regulating the accrual and long term stabilization of soil organic matter are still unclear. By integrating lab to field studies we aim to identify the molecules, organisms and metabolic pathways that control the formation of molecules that contribute to long term organic matter stabilization in bioenergy soils.
This study expands the current knowledge of host‐toxicant interactions and their associations with immune‐modulating members of the gut.
History of Breastfeeding but not Mode of Delivery shapes the Gut Microbiome in Childhood Camille Cioffi, MS
University of Oregon
Background. The naÃˉve neonatal gut is sensitive to early life experiences. Events during this critical developmental window may have life‐long impacts on the gut microbiota. Two experiences that have been associated with variation in the gut microbiome in infancy are mode of delivery and feeding practices (eg, breastfeeding). It remains unclear whether these early experiences are responsible for microbial differences beyond toddlerhood. Our study examined whether mode of delivery and infant feeding practices are associated with differences in the child and adolescent microbiome. To determine the impacts of these early experiences on the gut microbiome later in childhood, we used an adoption‐sibling design to compare genetically related siblings who were reared together or apart. Methods. Gut microbiome samples were collected from 73 children (M = 11 years, SD = 3 years, range = 3‐18 years). Parents reported on child breastfeeding history, age, sex, height, and weight. Mode of delivery was collected through medical records and phone interviews. Results. Negative binomial mixture models were conducted to identify whether mode of delivery and feeding practices were related to differences in phylum and genus‐level abundance of bacteria found in the gut of child participants. Covariates included age, sex, and body mass index. Genetic relatedness and rearing environment were accounted for as random effects. We observed a significant association between lack of breastfeeding during infancy and a greater number of the genus Bacteroides in stool in childhood and adolescence. Conclusion. Early formula feeding may impart lasting effects on the gut microbiome well into childhood.
Microbiomes and megafauna: exploring the relationships between disease, environment, and the microbiome Claire Couch
Oregon State University
In the past two decades, multiple studies have demonstrated intimate connections between commensal microbe communities and host health & disease in humans and laboratory animals. However, host‐microbiome relationships are poorly understood in most wildlife populations due to the inherent difficulties of wildlife studies, limiting our understanding of long‐term patterns and health outcomes of microbial dynamics. For this study, we took advantage of a unique high‐resolution, longitudinal dataset collected from a herd of African buffalo in Kruger National Park, South Africa. We examined the relationships of host traits, nutrition & disease with variation in the nasal & gut microbiome. Preliminary results indicate strong associations between the gut microbiome with environmental conditions and nutritional resource ability, and suggestive relationships between nasal microbiome composition and respiratory infections including bovine tuberculosis. and infection by respiratory pathogens including bovine tuberculosis. This study is unprecedented among wildlife microbiome studies in its scope, resolution, and duration, and we expect our results to substantially advance our understanding of how microbiomes function in a natural host population.
Children with autism and their typically‐developing siblings differ in exact sequence variants and predicted functions of stool‐associated microbes. Presented at ISME Maude David, PhD
Oregon State University
The existence of a link between the gut microbiome and Autism Spectrum Disorder (ASD) is well established in mice, but in human populations efforts to identify microbial biomarkers have been limited due to a lack of appropriately matched controls, stratification of participants within the autism spectrum, and sample size. To overcome these limitattions we crowdsourced the recruitment of families with age‐matched sibling pairs between 2‐7 years old (within two years of each other), where one child had a diagnosis of ASD and the other did not. Parents collected stool samples, provided a home video of their ASD children's natural social behavior, and responded online to diet and behavioral questionnaires. V4 16S amplicon sequencing of 117 samples (60 ASD and 57 controls) identified 21 Exact Sequence Variants (ESVs) that differed significantly between the two cohorts: 11 were found to be enriched in neurotypical children (six ESVs belonging to the Lachnospiraceae family), while ten were enriched in children with ASD (including Ruminococcaceae and Bacteroidaceae families). Summarizing the expected KEGG Orthologs of each predicted genome,
the taxonomic biomarkers associated with children with ASD can use amino acids as precursors for butyragenic pathways, potentially alterating the availability of neurotransmitters like glutamate and GABA
Center for Genome Research and Biocomputing at OSU Ed Davis, PhD
Oregon State University
The Center for Genome Research and Biocomputing at OSU provides services for DNA extraction, 16S and/or ITS amplification, Illumina MiSeq sequencing, and microbiome analysis of samples. We also will work with clients on research design, with particular focus on statistical power and limitations inherent in these types of studies. We recently received a contract from the Soil Health Institute to analyze the microbiomes of, in total, approximately 2000 soil samples from across the U.S., Canada, and Mexico.
PacBio sequencing of natural cyanobacterial blooms to study genome sequence and population structure Theo Dreher, PhD
Oregon State University
We report studies on the consensus genome sequences and the representation of SNPs in the populations of freshwater cyanobacterial blooms, finding a high degree of clonality in these populations that undergo annual boom and bust cycles. Freshwater cyanobacteria are increasingly afflicting lakes and reservoirs with blooms that can be toxic. An Anabaena bloom that occurs annually in Detroit Reservoir in the Cascade foothills is a producer of the toxin cylindrospermopsin. In June 2018, drinking water for the City of Salem, which is derived from Detroit Reservoir, was contaminated with cyanotoxins. We have determined the consensus genome sequence of Anabaena sp. DET69 from that bloom by PacBio sequencing of the uncultured bloom population. Illumina paired‐end libraries from the same sample, and from samples of blooms from preceding years, have been used to identify the genetic variation within a single population and between blooms in different years. The results will allow inferences on the diversity, dynamics, and possibly year‐to‐year evolution of these cyanobacterial populations.
Omics‐guided genome remodeling to promote productivity, evolutionary robustness, and biocontainment Rob Egbert, PhD
Pacific Northwest National Laboratory
As advances in microbial engineering work to meet goals in sustainable bioproduction, cell‐based therapeutics, and environmental monitoring, engineered functions often cause poor growth in the microbial host. Growth defects incurred from high expression of heterologous proteins reduce host productivity and leave engineered populations vulnerable to displacement by nonfunctional mutants. Further, culturing microbial cultures in controlled environments such as a bioreactor causes the expression of genes that are unnecessary for host or circuit function, leaving a significant fraction of the proteome dispensable. We are developing proteomics‐guided genome remodeling strategies to increase cellular capacity to express synthetic DNA circuits and heterologous biosynthetic pathways. This work includes cellular capacity optimization in a collection of massive genome deletion E. coli variants as well as cross‐evaluation of bacteria adapted to human gut, freshwater aquatic and plant rhizosphere environments. We expect this work to inform general genome remodeling strategies to eliminate the dispensable proteome while maintaining physiological robustness, leading to a better understanding of cellular responses to engineered loads and control of the longevity of engineered functions in complex environments.
Characterization of the stool microbiome in Latino, pre‐school children by weight status and time Presented at PAS 2018 Alex Foster, MD, MPH
Oregon Health & Science University
Background: Variations in microbiome composition and relative diversity have been found to be associated with weight status in early childhood. Most studies have been cross‐sectional and few clinical studies have examined microbiome changes in children in association with weight and diet change. Methods: Obese, pre‐school (2‐5‐year‐old), Latino children provided stool samples at baseline and six‐months into a behavioral intervention designed to improve their weight status. Unrelated, normal weight children from also provided stool samples at baseline. Stool community DNA was isolated, and the V1‐V3 region of the16S rRNA gene was sequenced. Estimates of within sample diversity (i.e., alpha diversity) were calculated on operational taxonomic unit (OTU) count data, and the Firmicutes:Bacteroidetes (F:B) ratio
Commensal orthologs of the human autoantigen Ro60 as triggers of autoimmunity in lupus Presented at Society for Investigative Dermatology meeting, American College of Rheumatology meeting Teri Greiling, MD, PhD
Oregon Health & Science University
The earliest autoantibodies in lupus are directed against the RNA binding autoantigen Ro60, but the triggers against this evolutionarily conserved antigen remain elusive. We identified Ro60 orthologs in a subset of human skin, oral, and gut commensal bacterial species and confirmed the presence of these orthologs in patients with lupus and healthy controls. Thus, we hypothesized that commensal Ro60 orthologs may trigger autoimmunity via cross‐reactivity in genetically susceptible individuals. Sera from human anti‐Ro60–positive lupus patients immunoprecipitated commensal Ro60 ribonucleoproteins. Human Ro60 autoantigen–specific CD4 memory T cell clones from lupus patients were activated by skin and mucosal Ro60‐containing bacteria, supporting T cell cross‐reactivity in humans. Further, germ‐free mice spontaneously initiated anti‐human Ro60 T and B cell responses and developed glomerular immune complex deposits after monocolonization with a Ro60 ortholog–containing gut commensal, linking anti‐Ro commensal responses in vivo with the production of human Ro60 autoantibodies and signs of autoimmunity. Together, these data support that colonization with autoantigen ortholog‐producing commensal species may initiate and sustain chronic autoimmunity in genetically predisposed individuals. The concept of commensal ortholog cross‐reactivity may apply more broadly to autoimmune diseases and lead to novel treatment approaches aimed at defined commensal species.
Transkingdom networks as a tool to uncover host‐microbiota interactions in metabolic disease Manoj Gurung, PhD
Oregon State University
During the last decade it became clear that host‐associated microbes play critical role in the pathogenesis of different diseases. However, a major challenge is to find which ones of the hundreds of microbial species or their products affect which specific host functions and vice versa. To address this problem, we have developed a new approach named analysis of transkingdom networks, which connects a mammalian host and microbiota genes or taxa. Building a transkingdom network requires establishing microbial and host gene expression networks separately and then integrating those two networks by edges that correspond to potential causal relations. The established predictions are then tested experimentally at the OSU Germfree/Gnotobiotic Mouse Core by colonizing mice with specific members of microbiota. We currently investigate transkingdom networks in a model of diet‐induced metabolic syndrome. In this case, we integrated gut microbiome with gene expression network encompassing major metabolic organs, such as liver, fat, muscle and intestine. Some critical inferences from these multi‐organ analyses are being validated. Thus, interrogation of transkingdom networks represents an effective method to reveal causal players in host‐microbiota interactions.
THE ENTERIC NERVOUS SYSTEM CONTROLS MICROBIAL INDUCED INFLAMMATION BY MODULATING INTESTINAL MOTILITY AND PERMEABILITY Presented at Federation of Neurogastroenterology and Motility (FNM) 2018 Kristi Hamilton, PhD
University of Oregon
OBJECTIVE: Our goal is to understand mechanisms by which the enteric nervous system (ENS) modulates interactions between intestine‐resident microbes and the intestinal tract. Zebrafish is an ideal model to study host‐microbe interactions due to the ease of deriving hundreds of genetically related individuals germ‐free (GF), the transparency of larval stages enabling live imaging, and the ease of mutagenesis and transgenesis. The ENS innervates the intestinal tract and controls many aspects of intestinal health, including motility and barrier function. Intestinal health can also be significantly affected by the resident microbiota. By studying sox10 mutants that lack an ENS, we showed that the ENS modulates the composition of the intestinal microbiota. This altered microbial community can cause intestinal inflammation as well as decreased barrier function, resulting in hyperpermeability. Probiotics, living microbes that provide benefit to the host and have been a suggested therapeutic for many gastrointestinal disorders, have been used to reduce or prevent intestinal hyperpermeability and alter intestinal motility. In this study, we investigated whether there is correlation between intestinal motility and intestinal inflammation, and whether a human probiotic is able to ameliorate the hyperpermeability that contributes to intestinal inflammation. METHODS: We used a custom‐built light
sheet microscope to measure intestinal motility and permeability in living wild type and sox10 mutant zebrafish larvae, and gnotobiogy techniques to investigate whether a beneficial microbe, Escherichia coli HS, could alleviate intestinal hyperpermeability. RESULTS: We discovered that the speed of intestinal contractions is significantly correlated with the level of intestinal inflammation in sox10 mutants. We also found that sox10 mutants have intestinal hyperpermeability that is ameliorated by inoculating them with E. coli HS. CONCLUSION: Our data suggest a mechanism by which host phenotype can influence microbial induced inflammation and a potential new avenue for therapy to improve intestinal barrier function and decrease intestinal inflammation.
The Microbiome of Kombucha SCOBY Presented at ASBC Keisha Rose Harrison
Oregon State University
Kombucha is a lightly carbonated tea that continues to disrupt the beverage market. The low‐sugar and low‐alcohol beverage has only been gaining in popularity in the United States over the last couple of years. What makes kombucha such a challenging beverage to make? The aerobic fermentation process driving kombucha production requires the action of a complex mixture of microorganisms. The flavor attributes and alcohol produced during the process are governed by the starter colony, a symbiotic culture of bacteria and yeast (SCOBY). The composition of the SCOBY is poorly understood which serves to limit the quality control of the commercial production of kombucha. The objective of this research is to profile a diverse array of commercial Kombucha SCOBY by establishing the microbiome. We hypothesize that the SCOBY ecology does not diverge with relative location and common microbial contributors persist. Through a collaboration with Kombucha Brewers International (KBI) we collected 92‐commercially provided kombucha biofilms. Prior to this study, the common contributors of the SCOBY ecology had not been well defined. Our results identified Gluconoacetobacter, Lactobacillus, Brettanomyces, and Starmerella as the most abundant taxa across the population independent of geographic origin. Five distinct styles of SCOBY were resolved and representative SCOBY from each group were selected for small batch fermentations. Final microbiome was profiled using high‐throughput sequencing to assess ecological community divergence.
Zinc Deficiency and Arsenic Elicit Combined Effects on the Gut Microbiome Presented at OSU CGRB Conference Emily Ho, PhD
Oregon State University
My research lab is interested in the impact of nutrients/bioactive food components on chronic disease development. We utilize animal models (rodent and zebrafish) and perform human intervention studies to address these questions. This specific project centers around how nutrient deficiencies may sensitive individuals to toxicological stresses. Chronic arsenic exposure affects 200 million people globally and presents serious health challenges. Dietary micronutrient deficiencies, which are often comorbid with chronic arsenic exposure, can enhance sensitivity to arsenic toxicity. However, the mechanisms that underpin this relationship are incompletely resolved. The gut microbiome interacts with host physiology to promote health, but micronutrient deficiencies can perturb these, which may lead to altered sensitivity to arsenic. We assessed the effect of arsenic exposure on microbial community composition of C57BL/ mice fed zinc adequate and marginally zinc deficient diets using 16S amplicon sequencing. We correlated taxonomic relative abundances with host DNA damage, adiponectin expression, and plasma zinc concentration to identify taxa that may mediate host physiological responses to arsenic exposure or zinc deficiency. We find that both arsenic exposure and zinc restriction alters microbiome diversity. In combination, arsenic and zinc restriction elicits stronger associations between arsenic concentration and microbial community structure. Arsenic exposure and zinc restriction also results in increased DNA damage and decreased plasma zinc. These physiological changes associate with the abundance of several taxa in the gut microbiome. These data indicate that marginal zinc deficiency sensitizes the microbiome to arsenic exposure and that the microbiome associates with some of the toxicological effects of arsenic.
Zebrafish model for intestinal cancer, nematode infecitons and the gut microbiome Michael Kent, PhD
Oregon State University
A collaboration between the Kent, Sharpton (Oregon State University) and Guillemin (University of Oregon) is investigating interactions between the intestinal microbiome, the parasitic nematode Pseudocapillaria tomentosa and a novel Mycoplasma sp. similar to Mycoplasma penetrans. To date, we have documented that the nematode causes
