Emerging from the pandemic into the sunshine, September 2021!
Some of the Allen-Vercoe lab, August 2018
Some of the Allen-Vercoe lab, September 2017
(Most of) the Allen-Vercoe Lab, Summer 2016
The Allen-Vercoe Lab, CBS BBQ, June 2014
The Allen-Vercoe lab, Gutsy Walk for the CCFC, June 2012
The Allen-Vercoe Lab Personnel
I work around the lab to keep everything in tip-top shape! I work closely on a project with the Yanomami, a group of hunter-gatherers in the Amazon rainforest that are not exposed to an industrial lifestyle. Traditional populations harbour microbes missing from Western populations which may have important consequences to human health. I am interested in approaching this project from the angle of the gut microbiota using cultivation techniques such as use of the Robogut system. The results of this project will help us better understand the historic role of the human gut microbiome, and if re-introducing lost species could improve the functionality of the gut microbiome of westernized populations.
Motto: "Just keep swimming!"
Hobbies: "Reading, knitting, catching up on corny TV shows"
Chris does all the things that keep the lab running smoothly, including animal work, biosafety, purchasing and accounting, shipping and receiving paperwork, due diligence and maintenance & repair of equipment. He also is the go-to person for batch and chemostat fermentation method development.
Motto: "If you're not going to do it right, don't bother!"
Hobbies: Watching bad reality TV shows, wind-gazing, fixing stuff.
firstname.lastname@example.org x 58007
Dr. Brendan Daisley
I am passionately interested in the underlying mechanisms of host-microbiota-xenobiotic interactions, big-data analytics in bioinformatics, and the development of microbial-based solutions to address large scale environmental concerns. In particular, one major research focus of mine is how beneficial microorganisms (especially bacteria, fungi, and archaea) can help support agricultural processes and global food security through improving the health of important pollinator insects, such as the honey bee.
Similar to humans, honey bees possess a co-evolved set of symbiotic microorganisms within their gut microbiota that help to promote health in multifaceted ways. While mounting evidence suggests that a loss and/or imbalance of these symbionts (i.e. microbial dysbiosis) is a predominant factor in honey bee population decline, it remains unclear what is driving these microbial changes, or the exact species involved. During my PhD studies in the Reid lab at Western University, I developed a bacterial delivery system for honey bees (known as the 'BioPatty') and demonstrated that hive supplementation with three immunostimulatory strains of lactobacilli (LX3 combo) could largely mitigate the immune deficits associated with antibiotic-induced microbiota damage. Despite the LX3 benefits, microbiota analysis with BEExact (a novel metaxonomic database tool for identification of microbial 'dark matter' in the hive) suggested that certain host-associated taxa were not recoverable and may be irreversibly lost following broad-spectrum antimicrobial exposure.
Following up on these findings, my postdoctoral research in the Allen-Vercoe lab focuses on two related goals. In brief, the first goal is to determine how common agri-industrial chemicals (which can possess antimicrobial properties comparable to that of antibiotics either unintentionally, or by-design in the case of certain pesticides) influence the honey bee gut microbiota, as well as the direct and/or indirect effects this may have on long-term host health outcomes. The second goal is to develop a microbiota restoration product containing a definable consortium of beneficial strains that are both necessary and sufficient for supporting optimal honey bee physiological functioning. Through this work, I ultimately hope to #savethebees and facilitate a sustainable future by developing basic frameworks of microbial management broadly relevant within apicultural and agricultural sectors.
Motto: “You can't fail if you never give up”
Hobbies: Nature walks, travelling, mushroom hunting, golfing, pine pollen collection
One of the most common in vivo models used in gastrointestinal and gut microbiome studies is the murine model. Mice possess a physiology and anatomy similar to humans, are inexpensive, have high reproductive rates and a short life cycle. However, a similarity mice and humans do not share is their gut microbiome. Compared to humans, mice differ genetically, consume a different diet, and are exposed to various environmental factors different to those found in most human environments. Each of these aspects shape the murine gut microbiome. Therefore, it is not surprising that differing mouse lines, or identical mouse lines with different housing conditions will display differing gut microbiomes. Collectively, these variations contribute to poor reproducibility and inconclusive results when using mice in lab experiments. As well, even mouse models which attempt to control differences in the microbiota fail to represent the true complexity and diversity found within the murine gastrointestinal tract. If we are to continue using mouse models as a proxy for human disease, one way to improve them may be to include a standardized murine-derived microbiome. My project, in collaboration with the Navarre Lab at the University of Toronto, aims to characterize the mouse gut microbiota, and to develop an in vitro model of the mouse colon in the Robogut that will help to standardize mouse models, and perhaps allow us to better understand their relevance to human health.
Motto: “Just be nice”
Hobbies: experimenting with foods, lifting things to be able to experiment with foods, and befriending dogs
My research involves the viral inhabitants of the human gut. Most of the living things in our gut are bacteria, so it comes as no surprise that most gut viruses infect bacteria, and bacteria only. Sometimes these bacterial viruses kill the cells they infect, and sometimes they 'upgrade' them with genetic novelties. In the latter case, the virus usually 'hides' inside the host-bacterium, piggy-backing on the success of its recently upgraded bacterial vessel. In most bacterial ecosystems, such as those in fresh water or soil, piggy-backing viruses are the minority. In the human gut, they are the majority.
Currently, I am seeking to understand how communities of piggy-backing viruses are formed in our gut, how they are maintained, and how they influence the bacterial populations that call our bowels 'home.' In other words, I am asking, “How did they get there? What can they do? How important are they for the fitness and health of a human?” I am doing this in collaboration with the Pride lab at UC San Diego.
To us, viruses are agents of disease. While many animal viruses are certainly to blame for a large portion of human suffering, many others are friendly to us. In fact, 7% of the human genome is composed of piggy-backing animal viruses that—like their bacteria-infecting counterparts—'hid' inside our ancestors' cells many thousands of years ago. These invaders have been hiding inside our cells for so long, they've forgotten how to get themselves out again! They are now permanent fixtures of our genetic code - the stuff that makes us 'us.' The same invasions are currently happening to the bacteria in our guts, but on a much faster and more dynamic scale. These invaders are abundant, adaptive, and unknown. If we are to truly understand what it means for a gastrointestinal ecosystem to be 'healthy,' we must first understand how these viruses influence the lives of their bacterial hosts.
Motto: "No crackers, Gromit! We've forgotten the crackers!"
Hobbies: Insect evolution, insect poems, insect neurology, viruses, rugby, hockey, rugby.
Fusobacterium nucleatum (Fn) is a common bacterial member of the human oral
microbiome—and it is an opportunist. When Fn is found elsewhere in the human body, the microbe is typically associated with disease, and colorectal cancer (CRC) is one such disease. In fact, the presence of Fn in the tissues can often predict a poor outcome. Unfortunately, we don't know much about how Fn causes disease, and whether all of the other microbes present in the colon, the colonic 'microbiota' influence this process.
To make a start in understanding disease processes, scientists often use animal or tissue culture models such as mice and 'organoids' (small pieces of tissue), respectively. In the case of mice, we don't yet understand whether Fn affects these animals in the same way it does humans. To address this, the first part of my research is aimed at understanding how well the mouse model of Fn disease matches what happens in human disease, at a molecular level. To do this, I will use cultured mouse cells and the equivalent human cells and infect them with Fn, then track the effects of infection at a molecular level using microscopy, to visualize the cells, and a technique called 'RNA-seq', which allows us to see how the cells are behaving.
The next part of my project is to understand how Fn might be influenced in its ability to cause disease by determining whether the colonic microbiota plays a role in infection. Members of the microbiota may be neutral bystanders to the process of Fn infection, but alternatively they may influence Fn by either helping or hindering the pathogenic process. I will carry out infection experiments in the presence of absence of selected microbes from the colon, and from this I should be able to see if there are certain microbes that, when present, may alter the course of Fn mediated disease.
Finally, since it is known that microbes communicate with each other using a chemical language, I am interested to find out whether Fn can respond to the language of the gut microbiota alone, and whether this is enough to alter the cause of infection. I will culture whole microbial ecosystems from the colons of both diseased and healthy people using a customized apparatus called a 'Robogut'. The Robogut mimics the human colonic environment, allowing us to grow most of the microbes present in a human colon, using, for example, poop as a starting point. Once the ecosystems are growing well, I will harvest some of this material and extract the molecules from the sample, without the microbes, and use this to see whether Fn can respond to this chemical language alone. If it does, there is great value in understanding which molecules Fn responds to in particular. This, and the outcomes of my other work will help in the development of novel therapies, diagnostic techniques or prevention strategies for CRC.
Motto: “Get $*it done!”
Hobbies: Cooking, writing, working weekends.
Bdellovibrio-and-Like Organisms (BALOs) are bacteria that have a unique lifestyle; they are predatory bacteria that attack and kill other bacterial species. The majority of the BALOs do this by squeezing inside the prey bacteria and using enzymes to dissolve the contents of the bacterial cell for use as food. One they have eaten their prey, the BALOs multiply and then pop out of the digested prey cell to continue their lifecycle on further prey. BALOs do not predate all bacterial cells, but only those with a double membrane - 'Gram negative' species.
There are several bacterial species that are known to play a role in the pathogenesis of colorectal cancer (CRC). These are certain forms of E. coli, Bacteroides fragilis, and Fusobacterium nucleatum, collectively known as 'oncomicrobes'. All of these species are Gram negative, and thus potentially vulnerable to attack by BALOs. Instead of treating a patient with broad-spectrum antibiotics, which risks promoting antibiotic resistance and damaging the microbial environment of the colon, could predatory bacteria be put to work to remove undesirable, cancer-promoting microbes from the colon?
The current goal of my research is thus to isolate BALOs from the environment and to then test them for their predation efficacy against oncomicrobes such as F. nucleatum. Those that are shown to be efficient predators will be further 'trained' to improve their predatory behaviour within conditions such as those found within the human gut (37°C and no oxygen). The hope is to find BALO strains which are effective predators against CRC-promoting oncomicrobes, and could be used therapeutically to reduce or remove such oncomicrobes from the colon without damaging the rest of the microbiota or the colon itself.
Motto: “Life moves pretty fast. If you don't stop and look around once in a while, you could miss it.”
Hobbies: Hockey, Squash, Skiing, Travelling, TV/Movie Thrillers
The rates of Type 2 diabetes (T2D) are on the rise globally, partly attributed to changing dietary habits trending towards more processed foods. These dietary shifts affect the collection of microbes found in the digestive tract called the human gut microbiome. Sequencing efforts have revealed differences between the gut microbiomes of those with T2D and healthy individuals. It has even been found that the functions of the T2D gut microbiome are different compared to the healthy gut microbiome and contribute to inflammation and T2D disease progression. These current studies have focused on adult participants with pre- and diagnosed T2D, however rates of T2D in adolescents are on the rise. In collaboration with Dr. Jayne Danska at SickKids Research Institute, stool samples from adolescents at risk of developing T2D have been collected. These samples will be the starting inoculum for the chemostat bioreactor system or 'Robogut' which is engineered to replicate conditions found in the human colon. Culturing the microbes in this way allows for community structure, metabolism, stability, and resilience to be monitored in a controlled system. The aim of this project is to gain a better understanding of the role gut microbes play in the development of T2D in adolescents. Hopefully this work will inform better treatment and prevention strategies in the future.
Motto: "There's lots of world out there!"
Hobbies: Graphic design, listening to podcasts, watching horror movies, gardening, and playing VR video games
My research goals are to characterize the gut microbiome of a remote indigenous people known as the Yanomami, and its link to their traditional diet and food acquisition. Historically, these people have been characterized and popularized as one of the last relatively isolated indigenous societies to have maintained their traditional active lifestyle of hunting-gathering, simple horticulture, and semi-nomadism.
Many Yanomami communities have limited to no exposure to Western stressors such as, but not limited to, antibiotics, processed foods, industrial toxins, and pollutants. A comprehensive study of the Yanomami gut microbiome as it correlates with diet and lifestyle will help further characterize a gut microbiome that is in homeostatic balance with the human host and will reveal what has been lost through Westernization. My research objectives are to use metagenomic and metabolomic approaches to assess the microbial diversity and function of stool samples obtained from Yanomami villagers; culture these unique communities in vitro using 'Robogut' bioreactors to assess the effects of different diets on microbial community structure and function; and isolate and characterize specific microbial isolates with unique characteristics absent in the Western gut microbiome.
In addition to the benefit this research may provide for global health, it will reinforce the importance of protecting the microbial diversity in the Amazon and its indigenous inhabitants. Furthermore, I have a familial responsibility to carry out this project as I am Yanomami and founder of the Good Project, a nonprofit that supports Yanomami programs in health, research, education, and cultural preservation. I commit to this research to advance our scientific understanding of how diet and lifestyle affects the human microbiome and keeps us healthy, and play a critical part in protecting the Amazon, its inhabitants, food systems, and microbes.
Motto: "90% of the game is half mental" - Yogi Berra
Hobbies: Hiking, camping, kayaking, exploration, mountaineering, playing baseball and dancing to 80s music in the living room when no one is watching
Visiting PhD student
(Host institution: University of Leeds, UK, PI: Dr. Phil Quirke).
Motto: Everyday's a school day.
Hobbies: ski mountaineering, waterskiing, running and cycling
Fusobacterium nucleatum and Parvimonas micra are anaerobic bacteria commonly found in the human oral cavity. Interestingly, both microbes are opportunistic pathogens, capable of migrating elsewhere in the body, where they have been associated with a variety of human infections and diseases. Notably, both F. nucleatum and P. micra are closely linked to the development of colorectal cancer (CRC). Despite recent research analyzing the roles that these microbes play in CRC and elucidating their impacts on host immune responses, the mechanisms by which F. nucleatum and P. micra contribute to the progression of CRC remains largely unknown.
In my research, I am interested in the potential impact of extracellular vesicles (EVs) on the development and progression of CRC. EVs are lipid-bound vesicles that are released from cells in all three domains of life (i.e., Archaea, Bacteria, and Eukarya) and travel into the extracellular space. EVs function in cell-cell communication via the transfer of specific cargo, such as nucleic acids and proteins, that can be internalized by recipient cells (e.g., via endocytosis) upon release into the extracellular space. As such, EVs play an important role in all biological processes, including in the development of cancer. In the context of cancer, cargo released from cancerous cells and their subsequent uptake by recipient cells can have numerous important effects, such as promoting recipient cell growth, increasing invasive or metastatic activity, and altering phenotypic expression. It is possible that EVs released from cancer cells may also impact microbes such as F. nucleatum and P. micra, and vice versa, which could play a role in the development and progression of CRC.
Motto: “A ship does not sail on yesterday's winds”
Hobbies: Hiking, skiing, biking, kayaking and baking banana bread
Type 1 Diabetes (T1D), a chronic autoimmune disease with usual onset in childhood, has seen global incidence rates rapidly increase with the development of disease occurring also at earlier ages. Many individuals who develop T1D carry predisposed genetic risk factors. However, very few genetically susceptible individuals develop T1D, indicating the potential for environmental factors to influence the pathogenesis of the disease. Breastmilk consumption during infancy is a factor that influences the risk of T1D development as studies have this has a protective role against disease development. Major components of breastmilk are human milk oligosaccharides (HMOs) which have various effects on infant development such as gut barrier promotion and host immune cell modulation. In breastfed infants, microorganisms that can use HMOs have a growth advantage over those that are unable to. Many Bifidobacterium strains utilize HMOs which helps them to proliferate in the infant gut. However, there is a lack of information in HMO utilization by other resident gut microbes, including T1D-associated gut microbes, as well as strain-level differences among bacterial species for HMO metabolism.
Recent findings from the Allen-Vercoe lab have shown various growth strategies used by a wide diversity of bacterial strains in the presence of pHMOs with many strains displaying HMO structure-based specificity. While most bacterial strains tested showed a growth advantage when treated with pHMOs, several microbes experienced pHMOs-induced growth inhibition, demonstrating a novel and seemingly specific anti-infective property of HMOs. My research will investigate how widespread pHMO inhibition is in gut microbiota—whether inhibition is strain-specific or occurs at broader ranks such as at the species and genus levels. I am also interested in identifying the mechanism of action through which pHMO inhibition occurs. This project is a collaboration with Dr. Jayne Danske at the Hospital for Sick Children and Dr. Lars Bode from the University of California, San Diego.
Motto: Trust the timing. Just because it's not happening right now, doesn't mean it never will.
Hobbies: Reading, Swimming, Watching documentaries, Calligraphy, Baking
Hobbies: DIY projects, cooking, baking, junior hockey, and caring for houseplants.
Motto: "It'll work out in the end."
Undergarduate Project Student
Motto: "Just keep swimming" -Dory, Finding Nemo
Hobbies: snuggling up on the couch to read, exploring local trails, dancing horribly to 2000's music, and cooking with friends
Undergraduate project student
Motto: Live, laugh, love
Hobbies: Thrifting, traveling, going to the gym, and being with friends!
Undergraduate project student
"We are all here on earth to help others; what on earth the others are here for I don't know" - W.H. Auden
Hobbies: reading, procrastinating, eating candy, boardgames, running
Motto: "Take the risk or lose the chance"
Hobbies: travelling, watching soccer games, and listening to Spanish music