Microbiology Symposium 2026

Poster session setup begins at 8:30 AM. Poster boards are 30 x 40 inches.

Morning Coffee (light refreshments provided)

Welcoming remarks will be delivered by the Symposium Chairs.  - Dr. Max Haggblom and Dr. Jeff Boyd.

Combination antiretroviral therapy (cART) has led to a decline in vertical HIV transmission and a growing population of infants who are exposed to HIV but uninfected (iHEU). Despite being uninfected, iHEU exhibit impaired growth, bone development, suboptimal responses to some vaccines, and neurodevelopmental delays compared to infants who are HIV-unexposed and uninfected (iHUU). The mechanism(s) underlying these adverse outcomes remain poorly understood. We hypothesized that differences in the very early-life gut microbiota of iHEU contribute directly to these developmental phenotypes.
To test this, we performed fecal microbiota transplantation experiments using stool collected from iHEU and iHUU neonates during the first week of life (days 4-7). Neonatal germ-free mice were transplanted with neonatal donor stool and assessed for growth, immune, brain and bone phenotypes at weaning. We also evaluated vaccine response using BCG, a TH1 inducing vaccine. 
We find that early-life HEU gut microbiota can causally drive adverse developmental outcomes, highlighting the importance of the pioneer microbiome in shaping child health.

The gut microbiome communicates with the brain to influence behaviors relevant to disorders such as autism spectrum disorder. However, the host mechanisms that translate microbial signals into behavioral outcomes remain poorly defined. Our work focuses on how intestinal microbes regulate signaling within the intestinal epithelium to shape both gut physiology and social behavior. We have identified a previously unrecognized source of oxytocin produced by intestinal epithelial cells and demonstrate that its secretion is modulated by microbial products. Ongoing studies are examining how epithelial oxytocin influences intestinal homeostasis and modulates social behavior. Together, this work defines a microbial-regulated enteric hormone relevant to gut physiology and brain function, positioning the intestinal epithelium as an active interface in gut-brain communication.

Agricultural pollution disproportionately burdens low-income and minority communities, contributing to health disparities through poorly understood mechanisms. Using hog dust extract (HDE) as a representative agricultural pollutant, this study investigated whether inhaled agricultural contaminants could disrupt intestinal homeostasis via the gut-lung axis. Intranasal HDE instillation in a murine model induced significant airway inflammation, marked by elevated bronchoalveolar lavage neutrophils and increased alveolar cellularity. HDE exposure also substantially increased intestinal permeability, elevated serum lipopolysaccharide concentrations and colonic TLR-4 expression, and reduced the barrier-protective commensal Akkermansia muciniphila. Additionally, HDE altered circulating metabolites involved in energy metabolism and immune regulation. These findings demonstrate that inhaled agricultural dust disrupts gut barrier integrity and microbial homeostasis, implicating the gut-lung axis as a key pathway through which occupational and environmental agricultural exposures may drive gastrointestinal and metabolic disease.

Dietary fibers, particularly fermentable fibers that resist digestion in the upper gastrointestinal tract and are subsequently metabolized by colonic microbes, have been shown to promote microbial diversity, maintain the abundance of core health-associated taxa, and help prevent or mitigate chronic metabolic diseases. However, fibers are not fermented uniformly in the gut, and distinct fiber molecules can therefore differentially modulate gut microbiota composition and function. Despite this, current dietary recommendations remain largely based on generalized intake guidelines (e.g., ~25–38 g/day) without distinguishing among fiber types or accounting for structural variation in their chemical composition. In our current study, we demonstrate that even subtle differences in fiber structure can influence community assembly, microbial division of labor, and organism-level metabolic responses. These findings underscore the importance of considering fine structural features and functional properties when using dietary fibers as prebiotic supplements and support the development of precision strategies for gut microbiome modulation.

Lunch will be provided in Trayes Hall, with priority given to registered attendees.

Antimicrobial-resistant and susceptible Klebsiella pneumoniae (Kp) are major causes of pneumonia and mortality in healthcare settings. We previously demonstrated that Kp evades airway immunity by reprogramming host metabolism, inducing mitochondrial oxidative phosphorylation (OXPHOS) and reactive oxygen species (ROS) production. This oxidant-rich milieu promotes accumulation of immunosuppressive myeloid cells that fail to clear Kp. We hypothesized that a ketogenic diet would favor immune clearance of Kp through host metabolic alterations, as diet-induced ketones may enhance immune cell bioenergetics and effector function.

Using a mouse pneumonia model, C57BL/6 mice fed a ketogenic diet showed reduced pulmonary Kp burden and improved survival compared with control diet-fed mice. Elevated levels of ketones in blood and airway fluid confirmed their systemic distribution. Ketogenic diet-fed mice exhibited increased pulmonary neutrophils, monocytes, and lymphocytes. Protection depended on neutrophils, as anti-Ly6G depletion reversed bacterial control, while Rag1 deficiency did not. Direct ketone administration reproduced the protective effect of the diet, highlighting ketone-supported neutrophil immunity in Kp clearance.

The Hargarten Lab is interested in understanding why some people develop severe disease when they encounter fungi and others don’t through studying human infections with Cryptococcus. Cryptococcosis primarily affects individuals with advanced immunosuppression, including those with HIV/AIDS, solid organ transplants, or prolonged corticosteroid exposure; however, little is known about why otherwise healthy persons develop severe disease. In the present studies, the largest cohort of previously healthy cryptococcosis patients were investigated to determine underlying immune deficiencies leading to susceptibility during primary infection and exuberant neuroinflammation during the post-infection period. Our goal is to utilize this information to both inform patient risk stratification and develop precision medicine approaches to restore host immunity and minimize post-infectious inflammation. Through whole-exome sequencing analysis of this patient cohort, we recently identified clusters of potentially deleterious genetic defects in patients that fall within biological and immunological pathways previously unexplored in the context of fungal disease, including MTOR signaling. Ongoing experiments, utilizing MTOR-flox mice and human cells, aim to further elucidate MTOR's role in immunity and the unique susceptibility to this important fungal pathogen. Additionally, through transcriptional analysis of patient cerebral spinal fluid we have identified the predominant pathway underlying post-infection neuroinflammation in this cohort, which can be successfully inhibited to improve clinical response.

Selected posters will be presented as flash talks.

Coffee Break – light refreshments provided

The ability to adapt to a changing and sometimes adverse environment is a fundamental and general property of any living system. It ensures survival. A mechanistic understanding of stress responses is therefore essential for deciphering the molecular logic of life in both the healthy and the diseased state. Here I will describe our work on the regulation of the RpoS general stress response in Escherichia coli and related species, focusing on the ATP-dependent proteolysis of RpoS by ClpXP, particularly on RssB, a ClpXP adaptor of exquisite specificity, and on its bidirectional regulation by post-translational modifications and anti-adaptor proteins that are stress-inducible and specialize the response dependent on specific stress signals.

Polymyxins are last-resort antibiotics that are used to treat multidrug-resistant (MDR) Gram-negative (GN) infections. Polymyxins associate with the outer bacterial membrane through electrostatic interactions with the phosphate groups of Lipid A. GN bacteria modify Lipid A in their membranes by adding diverse chemical moieties, leading to resistance against antimicrobial agents. We have recently elucidated the structure of two membrane enzymes that enable polymyxin resistance: the polyprenol phosphate glycosyltransferase ArnC that loads the L-Ara4N sugar onto the lipidic carrier undecaprenyl phosphate, and the aminoarabinose transferase ArnT that decorates Lipid A with the L-Ara4N sugar. We combine structural information with molecular dynamics simulations, microscale thermophoresis and polymyxin growth assays to develop a detailed understanding of the structural basis of catalysis in the above enzymes. Our program aims to characterize the basic biological functionality of these enzymes and enable targeted drug discovery to prevent or reverse polymyxin resistance in GN bacteria.

All around the country, commercial facilities rearing Zophobas morio "superworms" reported mass mortality of their insects with a consistent set of signs and symptoms. We used cryo-electron microscopy (cryo-EM) as a sequencing- and culturing-independent diagnostic tool to discover a new virus and identify it as the causative agent of Zophobas morio black wasting. We confirmed the etiology by fulfilling Koch's postulates, characterized the structure and sequence of various strains from around the country, and developed a prototype vaccination strategy. Towards extending these methods to diagnostic cryo-EM in man, we achieved unknown virus identification from cryo-ET from as little as one virus-infected cell.

Closing remarks will be delivered by the Symposium Chairs at the conclusion of the symposium.