Derrick Samuelson, Ph.D.
LSU Health Sciences Center New Orleans
Dr. Samuelson graduated from Montana State University with a B.Sc. in microbiology, and then joined the laboratory of Dr. Konkel in 2009 at Washington State University for his graduate studies. After completion of my Ph.D. he joined the laboratory of Drs. Shellito and Welsh at Louisiana State University Health Sciences Center New Orleans as a postdoctoral researcher. In 2016, Dr. Samuelson received the LA CaTS Meritorious Scholar award. His research interests are in microbiology, host-pathogen interactions, and immunology. Dr. Samuelson’s research began with the study of the skin-resident bacterial flora found on mice and transitioned to the study of bacterial-host interactions of the NIAID category B priority pathogen Campylobacter jejuni with a focus on the identification and characterization of C. jejuni virulence factors. This work led to the characterization of a novel Campylobacter invasion antigen (Cia), termed CiaD. Currently, his research is focused on the development of a live oral vaccine against Pneumocystis pneumonia, understanding the influences of the intestinal microbiota on pulmonary infection and immunity in immunocompromised individuals, and determining the mechanisms by which alcohol-induced intestinal dysbiosis impairs pulmonary host defense against Klebsiella pneumoniae.
Publications to Highlight:
Samuelson DR, Shellito JE, Maffei VJ, Tague ED, Campagna SR, Blanchard EE, et al. (2017) Alcohol-associated intestinal dysbiosis impairs pulmonary host defense against Klebsiella pneumoniae. PLoS Pathog 13(6): e1006426. https://doi.org/10.1371/journal.ppat.1006426.
Samuelson, D.R., de la Rua N.M., Charles T.P., Taylor C.M., Blanchard IV E., Meng L., et al. (2016) Analysis of the intestinal microbial community and inferred functional capacities during the host response to Pneumocystis pneumonia. Experimental lung research. 1-15. ePub Date: 12/7/2016.
LA CaTS Meritorious Scholar Project:
Alcohol use disorders (AUD) are an established risk factor for bacterial pneumonia. Further, alcohol consumption perturbs the normal intestinal microbial communities. Intestinal microbiota dysbiosis has been linked to impaired pulmonary host defense, however the role of alcohol-associated intestinal dysbiosis on pulmonary host defense is unknown. The project was to determine if alcohol-induced changes to the intestinal microbial community effect the host immune response to pulmonary bacterial infections. Specifically, the goal is to evaluate the role of alcohol-induced changes to the intestinal microbiota on pulmonary immune responses and susceptibility to Klebsiella pneumonia. The goal of this project is to describe the role of alcohol-related immune defects and its influence in alcohol using patient’s predisposition to respiratory bacterial pneumonia. The results of hs LA CaTS project have been recently published in PLoS Pathogens (https://doi.org/10.1371/journal.ppat.1006426). Briefly, we used an innovative model system to examine the role of alcohol-mediated intestinal dysbiosis on pulmonary host defense against respiratory infection with Klebsiella pneumoniae, independent of direct alcohol toxicity. He found that alcohol-mediated dysbiosis significantly increases host susceptibility to K. pneumoniae infection, independent of prevailing alcohol consumption. Alcohol-dysbiosis was associated with an altered T-cell responses in both the lung and intestinal tract following Klebsiella infection. Alcohol dysbiosis also lead to increased pulmonary inflammation, as well as intestinal inflammation and damage. The study demonstrates that alcohol-mediated dysbiosis impacts host defense and contributes to the impaired host defense against pneumonia frequently seen in alcohol abusers, and thus shifts conventional understanding of mechanisms of host defense impacted by alcohol. Characterization of microbial populations and metabolic products that regulate the immune system during harmful alcohol use may reveal novel therapeutic targets, as well as host-specific microbial communities that may be central to alcohol-mediated alterations in host defense.