Research and Publications
Research and Publications
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In the Keogh Lab, we investigate how bacterial pathogens persist in chronic wound infections, particularly in individuals with diabetes. These wounds are marked by inflammation, poor circulation, and altered immune function, that enables certain microbes to colonize, survive, and resist clearance. Our research focuses on understanding how these bacteria adapt to wound conditions, how they interact with host immune cells, and how co-infecting microbes influence disease outcomes. We aim to improve strategies for managing infections that fail to heal, with the broad goal of reducing complications and improving outcomes for patients with chronic wounds. Our lab integrates perspectives from microbiology, immunology, and microbial ecology, and we are committed to collaborative, rigorous training at the intersection of basic and translational science.
In the Keogh Lab, we investigate how bacterial pathogens persist in chronic wound infections, particularly in individuals with diabetes. These wounds are marked by inflammation, poor circulation, and altered immune function, that enables certain microbes to colonize, survive, and resist clearance. Our research focuses on understanding how these bacteria adapt to wound conditions, how they interact with host immune cells, and how co-infecting microbes influence disease outcomes. We aim to improve strategies for managing infections that fail to heal, with the broad goal of reducing complications and improving outcomes for patients with chronic wounds. Our lab integrates perspectives from microbiology, immunology, and microbial ecology, and we are committed to collaborative, rigorous training at the intersection of basic and translational science.
Specific Projects
Specific Projects
Bacterial Adaptation in the Chronic Wound Microenvironment
Bacterial Adaptation in the Chronic Wound Microenvironment
The diabetic wound microenvironment is very inflammatory, with high levels of reactive oxygen and nitrogen species, as well as large numbers of immune cells present. Bacteria need to adapt to overcome this harsh environment in order to survive in infection. Our lab focuses on the Gram-positive species Streptococcus agalactiae, also known as Group B Streptococcus (GBS) and Staphylococcus aureus, two of the most frequently isolated bacteria from diabetic wound infections. Specifically, we are interested in how these bacteria adapt over the course of diabetic wound infection on the genotypic and phenotypic level. We focus on identifying regulatory pathways and genetic modifications that support persistence in vivo.
Host–Pathogen Interactions and Immune Dysfunction
Host–Pathogen Interactions and Immune Dysfunction
Diabetes impairs multiple aspects of the innate immune response, including neutrophil recruitment, antimicrobial activity, and inflammatory resolution. These changes impair the host's ability to control infection and contribute to the persistence of microbes such as GBS in chronic wounds. Our lab focuses how hyperglycemia alters neutrophil function, particularly in the context of tissue damage and microbial colonization. We are working to understand how these immune defects shape infection outcomes and to identify ways to restore effective host defense through alternative therapeutic strategies.
Polymicrobial Interactions and Infection Ecology
Polymicrobial Interactions and Infection Ecology
Chronic wounds are rarely colonized by a single pathogen. Instead, diverse microbial communities coexist and compete in ways that influence infection outcomes. Our lab investigates how microbial species interact during co-infection, with a focus on how interspecies communication, competition, and metabolic exchange impact bacterial survival and virulence. We use wound infection as a model to explore broader questions in microbial ecology: how microbes establish niches, adapt to spatial constraints, and respond to selective pressures within the host. These dynamics play a critical role in processes like biofilm formation, cooperative defense, and the emergence of antibiotic resistance.
Select Publications
Select Publications
Joyce LR, Akbari MS, Nguyen DT, Spencer BL, McIver K, Horswill AR, Doran KS#, and Keogh RA#. Global genome analysis identifies glycolipids and lipoteichoic acid alanylation as contributors to Group B streptococcal diabetic wound infection. Pre-print. DOI: https://doi.org/10.1101/2025.05.02.651901
Keogh RA, Huyvaert SH, Moore GE, Horswill AR, and Doran KS. Characterization of Gram-positive Bacteria Isolated From Diabetic Foot Ulcer Debridement Tissue in Colorado. 2024. FEMS Microbe. DOI: 10.1093/femsmc/xtae013
Akbari MS*, Keogh RA*, Radin JN, Sanchez-Rosario Y, Johnson MDL, Horswill AR, Kehl-Fie TE, Burcham LR, and Doran KS. 2023. The impact of nutritional immunity on Group B streptococcal pathogenesis during wound infection. DOI: 10.1128/mbio.00304-23
Keogh RA, Doran KS. 2023. Group B Streptococcus and Diabetes: Finding the Sweet Spot. PLOS Pathogens. PLoS Pathogens. DOI: 10.1371/journal.ppat.1011133
Keogh RA, Haeberle AH, Langouet-Astrie CJ, Kavanaugh JS, Schmidt EP, Moore GE, Horswill AH, Doran KS. 2022. Group B Streptococcus adaptation promotes hyper-inflammation in the diabetic wound environment. Science Advances. DOI: 10.1126/sciadv.add3221
Burcham LR, Akbari MS, Alhajjar N, Keogh RA, Radin JN, Kehl-Fie TE, Belew AT, El-Sayed NM, McIver KS, Doran KS. 2022. Genomic analyses identify manganese homeostasis as a driver of Group B Streptococcal vaginal colonization. mBio. DOI: 10.1128/mbio.00985-22
Keogh RA*, Spencer BL*, Sorensen HS, Zapf RL, Briaud P, Doran KS#, and Carroll RK#. 2021. Global annotation, expression analysis, and stability of sRNAs in Group B Streptococcus. mBio. DOI: https://doi.org/10.1128/mBio.02803-21
For a complete list of publications see: https://www.ncbi.nlm.nih.gov/myncbi/1TCL-aLJCUZAH/bibliography/public/
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