Education

B.S. Microbiology, Clemson University, 2013
Ph.D. Biological Sciences, University of South Carolina, 2019

Training

NIH PREP Scholar, University of South Carolina, 2014-2015
Postdoctoral Fellowship in Immunology, University of South Carolina School of Medicine, 2019-2022

Biography

Dr. Kiesha Wilson is an Assistant Professor in the Department of Pathology, Immunology, & Microbiology at the University of South Carolina School of Medicine. She grew up in West Columbia, South Carolina, where a middle school field trip to Lexington Medical'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 a brief tenure in industry before she returned to research at the University of South Carolina through the Postbaccalaureate Research Education Program (PREP).

She then earned her Ph.D. in biological sciences from the University of South Carolina's Department of Biological Sciences. Her doctoral work led to the discovery of 4 different species of bacteriophage. Dr. Wilson 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. During this time, she took a brief hiatus from academia and returned to industry. Her research on acute respiratory distress syndrome and treatments with phytochemicals was subsequently awarded the NIH K99/R00 pathway-to-independence MOSAIC award, advancing her work and allowing her to return to academia.

She joined the University of South Carolina School of Medicine PMI department in 2023 as a faculty member and an Assistant Professor. Her research now focuses on understanding how epigenetic, microbial, and metabolic pathways influence immune responses and disease severity in acute respiratory distress syndrome (ARDS), with a particular emphasis on sex-specific mechanisms. Outside of the lab, Dr. Wilson is committed to promoting diversity in STEM.

Research

Role of Macrophages in CBD attenuation of SEB induced ARDS - R00GM147910
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.

Impact of Bacteroides on ARDS
Severe cases of Acute Respiratory Distress Syndrome (ARDS) and sepsis are characterized by excessive pulmonary inflammation and epithelial–endothelial barrier damage, leading to respiratory failure and high mortality. Understanding the underlying immune–microbial mechanisms that exacerbate lung injury is essential for developing novel therapeutic interventions. Increasing evidence suggests that gut microbiota play a pivotal role in shaping systemic and pulmonary immune responses through the gut–lung axis. Our recent findings identified Bacteroides acidifaciens (BA), a commensal gut bacterium, as a critical regulator of inflammatory responses in ARDS. In our pre-clinical studies, an increase in BA abundance following lung injury was associated with worsened disease outcomes, including enhanced neutrophil infiltration, elevated cytotoxic T cell activity, and increased inflammatory cytokine production. Multi-omics analyses—integrating 16S rRNA sequencing, untargeted metabolomics, and transcriptomics—revealed that BA alters bile acid metabolism, leading to activation of the aryl hydrocarbon receptor (AHR). AHR activation in turn drives a pro-inflammatory shift characterized by elevated IL-17 production and reduced IL-22–mediated tissue repair, particularly in female mice. We hypothesize that BA contributes to ARDS pathogenesis by metabolically reprogramming the gut–lung axis through bile acid–AHR signaling. Aim 1 will determine how BA colonization influences bile acid composition and systemic metabolite flux during ARDS. Aim 2 will define the immune cell populations and cytokine networks regulated by AHR activation in BA-enriched mice. Aim 3 will assess whether targeted reduction of BA using bacteriophage therapy or modulation of its metabolic products can attenuate inflammation and improve lung repair. This study will uncover microbial and metabolic pathways that exacerbate ARDS severity and evaluate Bacteroides acidifaciens as both a biomarker and potential therapeutic target for restoring immune balance in the lung.

Gut- Lung Axis
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.

Enhancing the utility of deer mice as an infectious disease model - R24AI186970
Deer mice (genus Peromyscus) are the most abundant mammals in North America. In biomedical research, their most prominent use is in the field of infectious diseases, because they are the natural reservoir of infectious agents such as Borrelia burgdorferi which causes Lyme disease, for Hantaviruses, Sin Nombre Virus, and SARS-CoV-2 that caused the COVID-19 pandemic. The University of South Carolina operates, for more than 40 years, the Peromyscus Genetic Stock Center (PGSC) that is charged with the mission of maintaining different stocks of Peromyscus, supplying them to outside investigators and exploiting deer mouse- related research. The present proposal addresses 3 major unmet needs of the Peromyscus community of researchers that impede the use of deer mice as a model and are related to the poor breeding program that does not enable rapid availability if deer mice to users, the lack of Peromyscus-specific antibodies, and the lack of readily access to breeding records for pedigree analyses. Here, we request funds to enhance the utility of deer mice as a model of relevance to NIAID’s interests by (1) strengthening the breeding capacities of the PGSC, (2) by developing specialized immunological reagents such as Peromyscus-specific antibodies, and (3) by curating our electronic databases and rendering them easily accessible to outside users. Plans for the project’s sustainability have been developed, and it is anticipated that upon completion it will be supported fully by the income generated.

Publications

• https://scholar.google.com/citations?user=Y0P5fdwAAAAJ&hl=en&oi=ao
• https://www.ncbi.nlm.nih.gov/myncbi/kiesha.wilson.1/bibliography/public/