The Elfenbein Lab is interested in how Salmonella causes disease and is transmitted between infected individuals. We use a combination of molecular genetics, cell culture, and animal infection models to understand the details underlying Salmonella biology in the gut and in the environment. Our overarching goal is to develop new treatments to ameliorate disease and prevent transmission in order to improve both human and animal health.
More information about our current projects can be found here:
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Intestinal and environmental metabolites influence Salmonella phenotypes
Non-typhoidal Salmonellae (NTS) can colonize and cause disease in all species of mammals. Disease is spread by consumption of contaminated food, water, or direct contact with individuals shedding the organism. In addition to colonizing mammals, NTS can also colonize birds and reptiles without causing disease, can colonize plants, and can create biofilms on abiotic surfaces to survive in the environment. The combination of broad host range and many strategies allowing for environmental persistence makes NTS very difficult to eradicate. Salmonella Typhimurium responds to host and microbial metabolites to stimulate either its virulence or biofilm paradigms. We hypothesize that metabolites present in the large intestine stimulate biofilm formation to prepare Salmonella for environmental survival. Ongoing projects in the laboratory study how byproducts of host and microbe amino acid metabolism alter Salmonella gene expression to facilitate its transition between the host and the environment.
Salmonella and the Neutrophil Respiratory Burst
Neutrophils are innate immune cells that are on the front line defending the host against invading pathogens. Unlike many other pathogens, Salmonella relies on neutrophils to colonize the gut. Neutrophilic inflammation kills competing resident microbes allowing Salmonella to grow in the gut to reach sufficient numbers for efficient transmission between hosts. Paradoxically, without functioning neutrophils, Salmonella infection causes lethal sepsis. We previously found that expression of Salmonella virulence genes (type-3 secretion system-1 and flagellar motility) are agonists of the neutrophil respiratory burst. We hypothesize that heterogeneity of Salmonella gene expression within the gut allows a portion of the population of Salmonella to thrive during intestinal inflammation. Our ongoing studies seek to understand how Salmonella modulates the magnitude of the neutrophil respiratory burst and other antimicrobial functions to develop therapeutic strategies that reduce Salmonella’s fitness in the gut.
Host-targeted therapeutics for enteric salmonellosis
Salmonella infections are a threat to both human and animal health. Multi-drug resistant infections are increasing at a dramatic rate, making it important to design new, non-antimicrobial strategies to eliminate Salmonella from the gut. Work in our laboratory is testing host-targeted therapeutics that have the potential to prevent Salmonella invasion into epithelial cells. We hypothesize that prevention of invasion will reduce collateral damage to the gut wall and will reduce Salmonella growth in the gut. Ultimately, we hope to reduce Salmonella shedding, environmental contamination, and transmission between animals.