The Microbes and Social Equity working group, and The University of Maine Institute of Medicine present a virtual symposium on:
“Living in a Microbial World”
June 5 – 9th, 2023.
Register here! It is free, and required.
Format: virtual meeting, Zoom platform.
The full program is here.
Session 5: MSE Member Research Showcase
Friday, June 9th, 11 am – 2:30 pm EDT.
Session hosts and organizers: Emily Wissel, Curtis Tilves, Sue Ishaq
Session Scope: MSE members will be sharing their own work in short presentations to showcase the variety of disciplines of our group. The presentation list will include students and non-researchers, and research on microbiomes, people, ecosystems, and more even if it is not related to microbes and/or social equity.
|Amber Benezra||The trillions of microbes in and on our bodies are determined by not only biology but also our social connections. Gut Anthro tells the fascinating story of how a sociocultural anthropologist developed a collaborative “anthropology of microbes” with a human microbial ecologist to address global health crises across disciplines. It asks: what would it mean for anthropology to act with science? Based partly at a preeminent U.S. lab studying the human microbiome, the Center for Genome Sciences at Washington University, and partly at a field site in Bangladesh studying infant malnutrition, the book examines how microbes travel between human guts in the “field” and in microbiome laboratories, influencing definitions of health and disease, and how the microbiome can change our views on evolution, agency, and life.|
My book Gut Anthro will be out May 9th!
|Melissa Manus||Social interactions shape the infant microbiome by providing opportunities for caregivers to spread bacteria through physical contact. With most research focused on the impact of maternal-infant contact on the infant gut microbiome, it is unclear how alloparents (i.e. caregivers other than the parents) influence the bacterial communities of infant body sites that are frequently contacted during bouts of caregiving, including the skin. To begin to understand how allocare may influence the diversity of the infant microbiome, detailed questionnaire data on infant-alloparent relationships and specific allocare behaviors were coupled with skin and fecal microbiome samples (4 body sites) from 48 infants living in Chicago, U.S.A. Data from 16S rRNA gene amplicon sequencing indicated that infant skin and fecal bacterial diversity showed a strong association to having female adult alloparents. Alloparental feeding and co-sleeping displayed stronger associations to infant bacterial diversity compared to playing or holding. There was variation in the magnitude and direction of these relationships across infant body sites. Bacterial relative abundances varied by infant-alloparent relationship and breastfeeding status. This study provides some of the first evidence of an association between allocare and infant bacterial diversity. The results suggest that infants’ exposure to bacteria from the social environment may differ based on infant-alloparent relationships and allocare behaviors. Since the microbiome influences immune system development, variation in allocare that impacts the diversity of infant bacterial communities may be an underexplored dimension of the social determinants of health in early life.|
|This talk will summarize work my laboratory is doing on environmental microbiomes. We primarily study nitrogen cycling and antimicrobial resistance in aquatic ecosystems, particularly in waters impacted by both urban and rural populations. Here I will describe a recent project attempting to use microbial source tracking to determine sources of nutrient inputs throughout a river network (the Mohawk/Teionontatátie), where we are combining quantification of fecal pathogens with detailed measurements of nitrogen compounds. We are particularly interested in determining the sources of urea and ammonium, since these can contribute to the extend or toxicity of harmful algal blooms in many freshwaters. I will also outline a project using metagenomic data to study antibiotic resistance gene abundance and diversity in urban estuary waters.|
|Ana Zuniga||Bacterial biosensor approaches for fast and cost-effective personal monitoring of potential gut biomarkers.|
Gut metabolites are pivotal mediators of host-microbiome interactions. The production of microbiome-derived metabolites can be affected by environmental chemicals, dietary substrate availability, and interindividual variability. Thus, they provide an essential window into human physiology and disease, where socio-environmental aspects also play a key role. However, current methods to monitor gut metabolites rely on heavy and expensive technologies such as liquid chromatography-mass spectrometry (LC-MS). In that context, robust, fast, field-deployable, and cost-effective strategies for monitoring fecal metabolites would support large-scale functional studies and routine monitoring of metabolite biomarkers associated with environmental exposures. Living cells are an attractive option to engineer biosensors due to their ability to detect and process many environmental signals and their self-replicating nature. Here we optimized a workflow for feces processing that supports metabolite detection using bacterial biosensors. We show that simple centrifugation and filtration steps remove host microbes and support reproducible preparation of a physiological-derived media retaining essential characteristics of human feces, such as matrix effects and endogenous metabolites. We measure the performance of bacterial biosensors for benzoate, lactate, anhydrotetracycline, and bile acids, and find that they are highly sensitive to fecal matrices. However, encapsulating the bacteria in hydrogel helps reduce this inhibitory effect. Finally, by detecting endogenous bile acids, we demonstrate that bacterial biosensors could be used for future metabolite monitoring in feces. This work lays the foundation for the optimization and use of bacterial biosensors in the monitoring of fecal biomarkers for a better characterization of individual environmental exposures.
|Marissa Kinney||Inflammatory bowel diseases (IBD) cause dysfunction of the gastrointestinal (GI) tract and can result in hospitalization, suffering and disruption to overall health. Recent work has demonstrated the anti-inflammatory capacity of a broccoli sprout-diet in artificially-induced GI inflammation in pathogen free C57BL/6 mice. Microbiota samples obtained from the GI tract of these mice will be used to study the presence and activity of broccoli glucosinolate hydrolysis to create microbial-sourced bioactives, to further understand the relationship between broccoli-diets and inflammation reduction. It is imperative to validate or replicate qPCR protocols which have been established for glucosinolate metabolism in Bacteroides thetaiotaomicron (B. theta), in other bacterial species. Additionally, this project will focus on developing new growth curve assays for glucosinolate metabolism, as these methods are lacking in published literature.|
|Lola Holcomb||Inflammatory Bowel Diseases (IBD) are chronic conditions characterized by inflammation of the gastrointestinal tract that heavily burden daily life, result in surgery or other complications, and disrupt the gut microbiome. How IBD influences gut microbial ecology, especially biogeographic patterns of microbial location, and how the gut microbiota can use diet components and microbial metabolites to mediate disease, are still poorly understood. Many studies on diet and IBD in mice use a chemically induced ulcerative colitis model, despite the availability of an immune-modulated Crohn’s Disease model. Interleukin-10-knockout (IL-10-ko) mice on a C57BL/6 background, beginning at age 4 or 7 weeks, were fed either a control diet or one containing 10% (w/w) raw broccoli sprouts which was high in the sprout-sourced anti-inflammatory sulforaphane. Diets began 7 days prior to inoculation with Helicobacter hepaticus, which triggers Crohn’s-like symptoms in these immune-impaired mice, and ran for two additional weeks. Key findings of this study suggest that the broccoli sprout diet increases sulforaphane concentration in plasma; decreases weight stagnation, fecal blood, and diarrhea associated with enterocolitis; and increases microbiota richness in the gut, especially in younger mice. Sprout diets resulted in some anatomically specific bacterial communities in younger mice, and reduced the prevalence and abundance of potentially pathogenic or otherwise-commensal bacteria which trigger inflammation in the IL-10 deficient mouse, for example, Escherichia coli and Helicobacter. Overall, the IL-10-ko mouse model is responsive to a raw broccoli sprout diet and represents an opportunity for more diet-host-microbiome research.|
|Timothy Hunt & Benjamin Hunt||Title: Missing microbes from early and later life are associated with chronic disease onset and treatment.|
Abstract: A review of an early-life microbe considered missing from the industrialized world that is associated with later-life chronic disease and a related microbe used to treat chronic disease.
|Johanna Holman||Inflammatory Bowel Diseases (IBD) are devastating conditions of the gastrointestinal tract with limited treatments, and dietary intervention may be effective, affordable, and safe for managing symptoms. Ongoing research has identified inactive compounds in broccoli sprouts, like glucoraphanin, and that mammalian gut microbiota play a role in metabolizing it to the anti-inflammatory sulforaphane. The objectives were to identify biogeographic location of participating microbiota and correlate that to health outcomes. We fed specific pathogen free C57BL/6 mice either a control diet or a 10% steamed broccoli sprout diet, and gave a three-cycle regimen of 2.5% dextran sodium sulfate (DSS) in drinking water over a 40-day experiment to simulate chronic, relapsing ulcerative colitis. We monitored body weight, fecal characteristics, fecal lipocalin, and sequenced bacterial communities from the contents and mucosa in the jejunum, cecum, and colon. Mice fed the broccoli sprout diet while receiving DSS performed better than mice fed the control diet while receiving DSS for all disease parameters, including significantly more weight gain (2-way ANOVA, p < 0.05), lower Disease Activity Index scores (2-way ANOVA, p < 0.001), and higher bacterial richness in all gut locations (linear regression model, p < 0.01 for all locations measured). Bacterial communities were assorted by gut location except in the mice receiving the control diet and DSS treatment (Beta-diversity, ANOVA, p < 0.05 for each). Importantly, our results suggested that broccoli sprout feeding completely abrogated the effects of DSS on gut microbiota, as bacterial communities were similar between mice receiving broccoli sprouts with and without DSS.|
|Emily Wissel||Background: The gut and vaginal microbiome both change over the course of a pregnancy and have been associated with many pregnancy complications. Pregnant individuals are more susceptible to urinary tract infections (UTIs), bacterial vaginosis (BV), and chlamydia infection. It is currently unclear if there are differences in the microbiome or the collection of antimicrobial resistance (AMR) genes for pregnant individuals who develop urogenital infections versus those who don’t. |
Methods: A subset of the data from the Emory University African American Vaginal, Oral, and Gut Microbiome in Pregnancy Cohort Study were sent for metagenomic sequencing (238 patients, rectal and vaginal swabs at 8-14 weeks & 24 – 30 weeks pregnancy). Taxonomic assignment was done with the metaphlan2 software tool, and AMR genes were detected with the AMR Finder Plus tool. 16S rRNA data from the same samples had taxonomic assignment with the PECAN and DADA2 tools. Associations between the microbiome and urogenital infections were analyzed with a linear decomposition model. Differences in the frequency of AMR genes was analyzed with a chi-squared test for independence.
Results: Collectively, this study finds that the gut and vaginal microbial communities are not significantly impacted by urogenital infections or their treatment. Specific microbes and AMR genes tend to be increased in those who developed urogenital infections compared to those who did not, however, these differences do not persist for the entire pregnancy. These findings should reassure most patients that being diagnosed with a urogenital infection and receiving antibiotic therapy for that infection will not have a significant, detrimental impact on their microbiome overall during pregnancy.