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The Wilson Lab

The Wilson Lab is run by Dr. Kiesha Wilson of the South Carolina School of Medicine Columbia PMI Department. The focus of the lab is on utilizing multi-omic approaches to understanding underlying mechanisms for multi-factors of acute respiratory distress syndrome.

Kiesha Wilson, Ph.D.

Kiesha Wilson Headshot

Dr. Kiesha Wilson is an Assistant Professor in the Department of Pathology, Immunology, & Microbiology at the University of South School of Medicine. Dr. Wilson grew up in West Columbia, South Carolina, where a middle school field trip to her local hospital’s pathology lab ignited her interest in science.

Her research experience began at Clemson University where she completed a B.S. in microbiology. The birth of her daughter led to her having a brief tenure in industry before returning to research at the University of South Carolina in the Postbaccalaureate Research Education Program (PREP).

She then earned her Ph.D. in biological sciences at the University of South Carolina in the Biological Sciences department. Her doctoral work led to the discovery of 4 different species of bacteriophage. Kiesha went on to complete postdoctoral training at the University of South Carolina School of Medicine where her research focused on inflammatory diseases and treatments with natural plant products. Her postdoctoral work was awarded the NIH K99/R00 pathway-to-independence MOSAIC award to advance this research on acute respiratory distress syndrome and treatments with phytochemicals.

She joined the University of South Carolina School of Medicine PMI department in 2023 as a faculty member and an Assistant Professor.

Outside of the lab, Dr. Wilson strives to promote diversity at the University of South Carolina School of Medicine Columbia by volunteering as a mentor for the Support for Minority Advancement in Research Training program (SMART). She also volunteers with other local organizations including the New Hope Leadership Academy and Empowerment Strategies, LLC, as a mentor to minority students from middle school to the undergraduate level. She is committed to promoting diversity in STEM.

About the Lab

Role of Macrophages in CBD Mediated Attenuation of SEB-Induced ARDS

Project One Diagram

Severe cases of Acute Respiratory Distress Syndrome (ARDS) and sepsis can be fatal due to pulmonary inflammation and destruction of the epithelial and endothelial cell lining. Understanding the mechanisms behind these diseases is vital to develop effective preventive and therapeutic strategies. Staphylococcus enterotoxin B (SEB)-induced ARDS mimics the cytokine storm, sepsis, and multiple organ failure presented in patients with severe COVID-19. It has been shown that the superantigen structure and sequence associated with the spike protein of SARS-CoV-2 is like that of SEB. In pre-clinical trials, treating ARDS with SEB drops survival rate to 0%. In our study, we found that Cannabidiol (CBD) administration following SEB treatment led to 100% survival indefinitely. Initial evaluation of whole single-cell sequencing data comparing lungs  with SEB induced ARDS illustrated that there was an increase in neutrophils, inflammatory macrophages, and proinflammatory cytokines (IL-1β and TNF-α) as well as a loss in lung epithelial cells. Single-cell RNA seq analysis of the toxin when treated with CBD has shown a decrease in the infiltration of inflammatory macrophage populations in the lung. Treatment with CBD also leads to increased survival probability, decreased proinflammatory cytokine production, and decreased bronchoconstriction caused by SEB. Using CCR2 KO we were able to visualize the pathogenesis of the disease in the absence of infiltrating “pro-inflammatory” macrophages. As a result, we found that disease severity was improved but not completely ameliorated. Utilizing SCID, we were able to identify whether macrophages independently of T cells would have the ability to induce ARDS caused by SEB. We found that there was an inflammatory response, however, not as severe as illustrated in the wild type. To continue to elucidate the mechanism by which CBD treatment led to amelioration of the inflammatory response, microRNA expression analysis was done that showed a significant decrease in expression of miR-124-3p and miR-298-5p in the SEB-exposed group which is directly associated with upregulation of TNF-α and IL-1β expression as well as macrophage activation gene, Cebpb. We hypothesized that CBD attenuates SEB-induced ARDS by miRNA dysregulation in lung-infiltrating cells, specifically by inducing miR-124-3p and miR-298-5pwhich downregulates Cebpb expression resulting in reduced activation of macrophages. Aim 1 will elucidate the role of resident and monocyte-derived macrophages in disease and the effect CBD on those subpopulations. Aim 2 will elucidate whether CBD affects Cebpb expression and the effects that miR-124-3p and miR-298-5p have on manifestation of disease. Aim 3 will determine the epigenetic factors regulating the expression of miR-124-3p and miR-298-5p. This study will explore CBD as a potential therapeutic for ARDS and/or sepsis-induced not only by SEB but other pathogens such as SARS-CoV-2.

Epigenetic/Transcriptomic Analysis of Multiple Causative Agents of ARDS

Project Two Diagram

Multiple factors both physical and microbial can induce ARDS. Being able to determine a global mechanism for ARDS induction will be helpful in the development of treatments that would be beneficial regardless of the causative agent. While previously I have induced ARDS with the use of an enterotoxin, I would like to explore other models of ARDS specifically Streptococcus pneumoniae, MHV-3, and Poly (I:C) induced ARDS to determine if the mechanism of disease is like that of my current model. Using these models, I can perform epigenetic studies like miRNA sequencing and histone modifications to determine if there is a targetable response that is observed in ARDS induced by multiple methods.

Effects of Phytochemicals on Neutrophil NETosis induced by ARDS

Project Three Diagram

One of the premier goals of my independent research is to elucidate the mechanisms of ARDS and how mechanistically different treatments might alleviate the fatal response. It is well known now that neutrophils produce extracellular traps (NETs) that heavily influence the hyperinflammatory response of viruses like SARS-CoV-2 that led to ARDS. In this study, I aim to investigate the effects of phytochemicals on neutrophil recruitment and NETosis. Utilizing the murine SEB-induced ARDS model, I will monitor neutrophil recruitment and activity via histology, flow cytometry, and cytokine production assays. This will be done in pre-clinical models treated with SEB/Cannabinoids. Next, I will focus particularly on the development of neutrophil NETs. Primary evaluations will be done using confocal imaging to visualize NET production following which, I will investigate the granule proteins, DNA, and histones produced in the lung with and without cannabinoid/SEB treatment. From the results, I would be able to infer whether cannabinoids affect NETosis and if so, the potential targets involved in regulation of NETosis.

Gut-lung axis

Project Four Diagram

The gut-lung axis is a concept that has been around for decades. Multiple groups have repeatedly illustrated that there is bi-directional crosstalk between the gut and lungs that may influence the prognosis of the disease. The over misuse of antibiotics and the increase in inflammatory diseases like colitis have made this topic even more interesting. In order to determine if previous dysregulation of the gut microbiome affects ARDS. I would like to approach this project from two directions. One method will be to treat ARDS with antibiotics and expose it to the virus a week later. I would expect to see some changes in disease development and progression. Alternatively, I also plan to bacterially induce chronic colitis and then introduce the virus to determine how gut inflammation and microbe dysregulation will affect disease prognosis. This will enhance the knowledge in the field and help to inspect why ARDS responses may differ from person to person.

 

Vedantam, P., Tzeng, T. R. J., Brown, A. K., Podila, R., Rao, A., & Staley, K. (2012). Binding of Escherichia coli to functionalized gold nanoparticles. Plasmonics7, 301-308.

Callahan, C. T., Wilson, K. M., & Ely, B. (2016). Characterization of the proteins associated with Caulobacter crescentus bacteriophage CbK particles. Current microbiology72, 75-80.

Scott, D. C., Scott, L., Wilson, K., Ross, K., Ingram, D., Lewter, T., ... & Ely, B. (2018). Complete genome sequence of a wild-type isolate of Caulobacter vibrioides strain CB2. Microbiology resource announcements7(17), 10-1128.

Wilson, K., & Ely, B. (2019). Analyses of four new Caulobacter Phicbkviruses indicate independent lineages. The Journal of General Virology100(2), 321.

Ely, B., Wilson, K., Ross, K., Ingram, D., Lewter, T., Herring, J., ... & Scott, D. (2019). Genome comparisons of wild isolates of Caulobacter crescentus reveal rates of inversion and horizontal gene transfer. Current microbiology76, 159-167.

Wilson, K. M., Miranda, K., Kaul, M., Nagarkatti, P. S., & Nagarkatti, M. (2020). Single cell profiling illustrates down-regulation of GM42031 in macrophages and microglia as a potential mechanism of neuroinflammation in transgenic GFAP-gp120 mice. The Journal of Immunology204(1_Supplement), 225-12.

Mohammed, A., FK Alghetaa, H., Miranda, K., Wilson, K., P. Singh, N., Cai, G., ... & Nagarkatti, M. (2020). Δ9-tetrahydrocannabinol prevents mortality from acute respiratory distress syndrome through the induction of apoptosis in immune cells, leading to cytokine storm suppression. International Journal of Molecular Sciences21(17), 6244.

Wilson, K., Zhu, F., Zheng, R., Chen, S., & Ely, B. (2020). Identification of proteins associated with two diverse Caulobacter phicbkvirus particles. Archives of virology165, 1995-2002.

Becker, W., Alrafas, H. R., Wilson, K., Miranda, K., Culpepper, C., Chatzistamou, I., ... & Nagarkatti, P. S. (2020). Activation of cannabinoid receptor 2 prevents colitis-associated colon cancer through myeloid cell de-activation upstream of IL-22 production. Iscience23(9).

Ely, B., Liese, J., Corley, S., Nguyen, D., Wilson, K., & Berrios, L. (2020). Novel Caulobacter bacteriophages illustrate the diversity of the podovirus genus Rauchvirus. Archives of virology165, 2549-2554.

Wilson, K. M., Cannon, A. S., Sultan, M., Nagarkatti, P., & Nagarkatti, M. (2021). A single-cell atlas of the lung mononuclear cell response in Staphylococcus Enterotoxin B-induced Acute Respiratory Distress Syndrome. The Journal of Immunology206(1_Supplement), 110-15.

Becker, W., Alrafas, H. R., Busbee, P. B., Walla, M. D., Wilson, K., Miranda, K., ... & Nagarkatti, P. S. (2021). Cannabinoid receptor activation on haematopoietic cells and enterocytes protects against colitis. Journal of Crohn's and Colitis15(6), 1032-1048.

Dopkins, N., Miranda, K., Wilson, K., Holloman, B. L., Nagarkatti, P., & Nagarkatti, M. (2021). Effects of orally administered cannabidiol on neuroinflammation and intestinal inflammation in the attenuation of experimental autoimmune encephalomyelitis. Journal of Neuroimmune Pharmacology, 1-18.

Sultan, M., Wilson, K., Abdulla, O. A., Busbee, P. B., Hall, A., Carter, T., ... & Nagarkatti, M. (2021). Endocannabinoid anandamide attenuates acute respiratory distress syndrome through modulation of microbiome in the gut-lung axis. Cells10(12), 3305.

Cannon, A. S., Holloman, B. L., Wilson, K., Miranda, K., Dopkins, N., Nagarkatti, P., & Nagarkatti, M. (2022). AhR Activation Leads to Attenuation of Murine Autoimmune Hepatitis: Single-Cell RNA-Seq Analysis Reveals Unique Immune Cell Phenotypes and Gene Expression Changes in the Liver. Frontiers in Immunology13, 899609.

Wilson, K., Nagarkatti, M., & Nagarakatti, P. (2023). CBD Treatment Improves Fatal Inflammatory Response Exhibited in SEB-Induced ARDS. Journal of Biological Chemistry, S172-S172.

Alghetaa, H., Mohammed, A., Singh, N., Wilson, K., Cai, G., Putluri, N., ... & Nagarkatti, P. (2023). Resveratrol attenuates staphylococcal enterotoxin B-activated immune cell metabolism via upregulation of miR-100 and suppression of mTOR signaling pathway. Frontiers in Pharmacology14, 1106733.

Holloman, B. L., Cannon, A., Wilson, K., Nagarkatti, P., & Nagarkatti, M. (2023). Aryl hydrocarbon receptor activation ameliorates acute respiratory distress syndrome through regulation of Th17 and Th22 cells in the lungs. MBio14(2), e03137-22.

Holloman, B. L., Cannon, A., Wilson, K., Singh, N., Nagarkatti, M., & Nagarkatti, P. (2023). Characterization of Chemotaxis-Associated Gene Dysregulation in Myeloid Cell Populations in the Lungs during Lipopolysaccharide-Mediated Acute Lung Injury. The Journal of Immunology210(12), 2016-2028.

The lab's main focus is to use molecular and multi-omics research to study acute respiratory distress syndrome (ARDS). We are interested in studying the role of macrophage plasticity in modulating various causative agents of acute respiratory distress syndrome and understanding the epigenetic factors that mediate disease pathogenesis. We use a combination of state-of-the-art methodologies, from lung function assessments to multiple next-generation sequencing tools in pre-clinical models.

Are you interested in joining the Wilson Lab? Reach out to director Kiesha Wilson, PhD at kiesha.wilson@uscmed.sc.edu to obtain a list of opportunities and how to apply.

Dr. Wilson’s doctoral work was recognized by ICTV!

 “New species of Caulobacter bacteriophage named after Dr. Bert Ely!” UofSC Biological Sciences News. February 24, 2021. https://www.sc.edu/study/colleges_schools/artsandsciences/biological_sciences/about/news/2021/news_ely_bacteriophages.php

Dr. Wilson receives K99/R00 transition award!

“Mosaic Scholars” NIGMS Training, Workforce Development, and Diversity, Career Development Awards. September 12, 2022. https://nigms.nih.gov/training/careerdev/Pages/mosaic-scholars.aspx

 


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