Urologic diseases interstitial cystitis (IC), overactive bladder (OAB), and urinary tract infection (UTI) affect tens of millions of people per year in the US alone. The human microbiome consists of a diverse community of bacteria (bacteriome) and viruses (virome) harbored in each individual that contributes to health and disease. Little is known about how the microbiome impacts urinary disorders. Using next-generation metagenomic sequencing, we characterized the urinary bacteriome and virome of patients with urinary disorders (IC, OAB, and UTI) and healthy controls. We show that the bacteriome was distinctly altered in patients by their respective urinary disorder. IC was characterized by a distinct prevalence of the genus Lactobacillus, while OAB was characterized by the genus Bacteroides, and UTI was characterized by Comamonas. IC, OAB, and UTI all also had significantly differed virome profiles from healthy individuals. In particular, we found that Lactobacillus phages were significantly associated with IC and Corynebacterium virus was associated with UTI samples, meanwhile no particular virus was correlated with OAB samples. Overall, we show that changes in the urinary microbiome are associated with incidence and spectrum of urinary diseases. These findings could lead to new microbiome modalities of treatment.

The microbiome and the immune system are known to work in conjunction to modulate the clearance of pathogens and tolerance of beneficial microbes. A growing area of research seeks to study the potential extent of the involvement of the microbiome in modulating and supporting the immune system during acute allograft rejection. It has been hypothesized that the localized microbiota in each organ produce metabolites that instigate inflammatory immune responses, but whether microbiota interactions precipitate acute allograft rejection is unknown. Therefore, this study focuses on microbiome shifts in the gut and kidney after inducing acute renal transplant rejection in order to implicate gut dysbiosis as a precursor or supporter of allograft rejection. This study also subsequently explores the use of an immune-modulating protein in order to determine differences in the outcome of transplant rejection and potential differences in intestinal microbial load. This experiment sought to induce rejection in BALB/c mice through the use of C57BL/6 mouse renal slivers. Microbiome abundance was analyzed in all experimental groups. Understanding the role of the microbiome in transplant rejection has vast clinical implications and has the potential to enhance pre- and post-operative treatment, and immune management and quality of life following organ transplant.

The microbiome and virome are known to interact within the human body which in turn modulates the health and disease of an individual. While these interactions have been largely studied in bodily sites such as the gastrointestinal tract, the microbiome and virome of the female genital tract (FGT) remains largely understudied. Within the virome exists DNA and RNA viruses which are known to infect both eukaryotes and prokaryotes. While existing virome research within the FGT has focused largely on eukaryote infecting viruses, a large proportion of the virome consists of uncharacterized bacteriophages known as “dark matter”. Due to the lack of a specific gene marker for viruses, which is essential in qPCR quantification of other populations such as bacteria, determination of viral abundance and virome characterization has been limited. However, the staining of viral DNA has been found effective in visualizing and enumerating virus-like particles within various specimens. In this study, we seek to determine viral abundance within the FGT utilizing SYBR Gold nucleic acid stain to visualize VLP present within a cohort of cervicovaginal lavage (CVL) samples. Given these results we intend to draw conclusions regarding the interactions between the FGT virome and viral abundance as well as sexual-reproductive health. Understanding the complex relationship of the virome within the female reproductive tract is likely to have remarkable clinical implications and has the potential to progress both the diagnostic and treatment aspects of female sexual and reproductive health.

Humans and their microbiota are in a symbiotic relationship. It is known that microbiale residents within and on human bodies have the potential to impact host physiology in both healthy and disease states. To date, little is known about the potential influence of the gut microbiome on the onset of nausea symptoms among cancer patients undergoing chemotherapy treatment. Chemotherapy-induced nausea (CIN) is a serious and common side effect. The CIN presentation is often coupled with other symptoms such as fatigue, sleep disturbance, depression, and anxiety. These symptoms both on an individual and collective level, cause negative impacts on patients’ health outcome as they challenge patients’ ability to tolerate and comply with chemotherapy. To understand the association between gut microbiome and CIN, we applied 16S rRNA amplicon sequencing to characterize the gut microbiome of breast cancer patients who reported nausea symptoms and those who reported no nausea symptoms. We hypothesize that the gut microbiome of patients who reported nausea symptoms is distinct from patients who reported no nausea. Our findings support this hypothesis, as the gut microbiome of nausea case was distinct from the no nausea cases. Specifically, we observed decreased abundance of Bacteroidetes in patients who reported nausea, while patients who reported no CIN had constant or increased abundance of Bacteroidetes. Overall, we showed that changes in the gut microbiota have an association with the occurrence of CIN symptoms among breast cancer patients receiving chemotherapy. These findings provide preliminary data for extensive research on the role of gut microbiome in CIN in the future.

Tropical peatlands play a critical role in global carbon storage and greenhouse gas flux, yet the role of microbial communities in these ecosystems remains poorly understood. Methane-oxidizing bacteria (MOB) are considered an efficient biological filter for methane and can mitigate its release into the atmosphere, facilitating an ecosystem’s capacity to become a net sink. Prokaryotic gene amplicon surveys targeting a unique biomarker instead of a universal one (i.e., 16S rRNA) can reveal a more comprehensive analysis of microbial communities with ecological functions (i.e., methanotrophy). The alpha subunit of particulate methane monooxygenase (pmoA) is commonly targeted as a phylogenetic biomarker for both aerobic and anaerobic MOB. Here, we tested three different primer sets and investigated their ability to assess methanotrophic diversity across three biogeochemically distinct tropical peatland sites in the Pastaza-Marañón foreland basin (PMFB) in western Amazonia. The results showed that sequencing using 16S rRNA and pmoA genes revealed differences in MOB taxonomic identification in 21 tropical peat soils. Beta diversity analysis of pmoA genes suggests that site location is not the main driver of differences in MOB community makeup. This work offers insight into the strengths and weaknesses of targeted gene amplicon surveys using 16S and pmoA from tropical peat soils as a case study.

Obesity increases the risk for colorectal cancer. In mice, a pro-obesity high-fat-diet (HFD) leads to an intestinal phenotype characterized by enhanced proliferation, numbers, function and tumor-initiating capacity of stem cells, the cell-of-origin for many intestinal cancers. This phenotype is driven by a lipid metabolism program facilitated by an intrinsic Peroxisome Proliferator-Activated Receptor/Fatty Acid Oxidation (PPAR/FAO) axis that senses and utilizes cellular lipids. However, the microbiome is a known regulator of lipid metabolism in the gut, but little is understood about how the gut commensals affect access to the lipids and alter stem cell function. Here, we use the long term HFD-fed mouse model to analyze the phenotypic changes in the intestinal stem cells (ISCs) after depletion of the gut microbiota. We find that the loss of the gut microbiome after four weeks of antibiotic treatment imposes significant changes in ISC function leading to reduced HFD ISC regenerative potential. These results indicate that the gut microbiome plays a crucial role in the lipid metabolic process which regulates and maintains the HFD ISC phenotype, and further suggests that the gut microbiome may augment the diet-induced tumor initiating capacity by altering the stem cell function.