About

Elizabeth Rose is an Assistant Clinical Professor at the College of Veterinary Medicine at NC State University. She is part of the Anatomic Pathology Hospital personnel. Her role involves clinical pathology, and she is involved in the department's activities related to anatomic pathology. Specific details about her research focus, background, or key contributions are not provided in the page text.

Research topics

• Biology
• Internal medicine
• Medicine
• Pathology
• Immunology
• Gastroenterology
• Bioinformatics
• Virology
• Genetics
• Cell biology

Selected publications

• Single-cell transcriptomics predict novel potential regulators of acute epithelial restitution in the ischemia-injured intestine

  UNC Libraries · 2026-05-06

  articleOpen access

  Intestinal ischemic injury damages the epithelial barrier predisposes patients to life-threatening sepsis unless that barrier is rapidly restored. There is an age-dependency of intestinal recovery in that neonates are the most susceptible to succumb to disease of the intestinal barrier versus older patients. We have developed a pig model that demonstrates age-dependent failure of intestinal barrier restitution in neonatal pigs which can be rescued by the direct application of juvenile pig mucosal tissue, but the mechanisms of rescue remain undefined. We hypothesized that by identifying a subpopulation of restituting enterocytes by their expression of cell migration transcriptional pathways, we can then predict novel upstream regulators of age-dependent restitution response programs. Superficial mucosal epithelial cells from recovering ischemic jejunum of juvenile pigs underwent single cell transcriptomics and predicted upstream regulator CSF-1 was interrogated in our model. A subcluster of absorptive enterocytes expressed several cell migration pathways key to restitution. Differentially expressed genes in this subcluster predicted their upstream regulation by colony stimulating factor-1 (CSF-1). We validated age-dependent induction of <em>CSF-1</em> by ischemia and documented that CSF-1 and CSF1R co-localized in ischemic juvenile, but not neonatal, wound-adjacent epithelial cells and in the restituted epithelium of juveniles and rescued neonates. Further, the CSF-1 blockade reduced restitution <em>in vitro</em>, and CSF-1 improved barrier function in injured neonatal pig in preliminary <em>ex vivo</em> experiments. These studies validate an approach to inform potential novel therapeutic targets, such as CSF-1, to improve outcomes in neonates with intestinal injury in a unique pig model.

  PublisherDOI

• Bile acid dependent attenuation of toxin mediated disease is independent of colonization resistance against <i>C. difficile</i>

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-12

  articleOpen access

  ABSTRACT Clostridioides difficile infection (CDI) is a severe antibiotic associated disease and a major cause of morbidity and mortality worldwide. CDI is thought to arise from the loss of protective gut microbes that mediate functions such as secondary bile acid metabolism and nutrient competition, yet the relative contributions of these mechanisms remain unclear. To determine how these processes influence C. difficile growth, virulence, and disease, we performed in vitro and in vivo experiments using two Clostridia strains previously associated with colonization resistance against C. difficile . Neither organism prevented colonization or growth through nutrient competition alone. In contrast, secondary bile acid metabolism significantly reduced toxin-mediated disease in vivo in a strain dependent manner. These findings demonstrate that secondary bile acid modulation is an important component of CDI prevention independent of nutrient competition and suggest that attenuating virulence, in addition to limiting colonization, may represent a key strategy for next-generation CDI therapeutics.

  PublisherOA PDFDOI

• Single-cell transcriptomics predict novel potential regulators of acute epithelial restitution in the ischemia-injured intestine

  American Journal of Physiology-Gastrointestinal and Liver Physiology · 2025-01-24

  articleOpen access1st authorCorresponding

  These studies validate an approach to identify and predict upstream regulation of restituting epithelium in a unique pig intestinal ischemic injury model. Identification of potential molecular mediators of restitution, such as CSF-1, will inform the development of targeted therapeutic interventions for the medical management of patients with ischemia-mediated intestinal injury.

  PublisherOA PDFDOI

• Congenital goiter in sibling goat kids

  Brazilian Journal of Veterinary Pathology · 2025-12-22

  articleOpen access

  History: Nine, adult, female Boer goats were presented to the University of California, Davis, Veterinary Medical Teaching Hospital for timed artificial insemination. To synchronize their estrous cycles, the owner gave each doe 7.5 mg dinoprost tromethamine (Lutalyse®) intramuscularly 12 hours prior to presentation and 24 hours prior to removal of the doe’s progesterone controlled intravaginal drug release device (EAZI-BREED™ CIDR®). Approximately 52 hours after prostaglandin administration, one of the does delivered two live kids, one female and one male, without complication. The neonates were unexpectedly premature by approximately two weeks. Both kids exhibited bilateral, smooth swelling at the laryngotracheal junction and generalized alopecia. Both kids were euthanized, and they were sent to the UC Davis Anatomic Pathology Service for necropsy.

  PublisherOA PDFDOI

• Structure-guided design of a synthetic bile acid that inhibits Clostridioides difficile TcdB toxin

  Nature Microbiology · 2025-11-18 · 1 citations

  article
  PublisherDOI

• Single-cell transcriptomics predict novel potential regulators of acute epithelial restitution in the ischemia-injured intestine

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-06-30

  preprintOpen access1st author

  ABSTRACT Intestinal ischemic injury damages the epithelial barrier predisposes patients to life-threatening sepsis unless that barrier is rapidly restored. There is an age-dependency of intestinal recovery in that neonates are the most susceptible to succumb to disease of the intestinal barrier versus older patients. We have developed a pig model that demonstrates age-dependent failure of intestinal barrier restitution in neonatal pigs which can be rescued by the direct application of juvenile pig mucosal tissue, but the mechanisms of rescue remain undefined. We hypothesized that by identifying a subpopulation of restituting enterocytes by their expression of cell migration transcriptional pathways, we can then predict novel upstream regulators of age-dependent restitution response programs. Superficial mucosal epithelial cells from recovering ischemic jejunum of juvenile pigs were processed for single cell RNA sequencing analysis, and predicted upstream regulators were assessed in a porcine intestinal epithelial cell line (IPEC-J2) and banked tissues. A subcluster of absorptive enterocytes expressed several cell migration pathways key to restitution. Differentially expressed genes in this subcluster predicted their upstream regulation included colony stimulating factor-1 (CSF-1). We validated age-dependent induction of CSF-1 by ischemia and documented that CSF-1 and CSF1R co-localized in ischemic juvenile, but not neonatal, wound-adjacent epithelial cells and in the restituted epithelium of juveniles and rescued (but not control) neonates. Further, the CSF1R inhibitor BLZ945 reduced restitution in scratch wounded IPEC-J2 cells. These studies validate an approach to inform potential novel therapeutic targets, such as CSF-1, to improve outcomes in neonates with intestinal injury in a unique pig model. NEW &amp; NOTEWORTHY These studies validate an approach to identify and predict upstream regulation of restituting epithelium in a unique pig intestinal ischemic injury model. Identification of potential molecular mediators of restitution, such as CSF-1, will inform the development of targeted therapeutic interventions for medical management of patients with ischemia-mediated intestinal injury.

  PublisherOA PDFDOI

• Single-cell transcriptomics predicts colony stimulating factor-1 regulation of age-dependent intestinal epithelial restitution

  Physiology · 2024-05-01

  article

  Intestinal diseases associated with ischemic injury, which damages the principal barrier against noxious luminal contents, result in unacceptably poor outcomes in newborns. Ischemia-induced loss of the intestinal epithelial barrier predisposes patients to life-threatening sepsis unless that barrier is rapidly restored. There is an age-dependency of intestinal recovery in that neonates are the most susceptible to succumb to disease of the intestinal barrier versus older patients. While this age-dependence in repair has not been demonstrated in traditional rodent models, we have developed a highly translational pig model of intestinal ischemic injury and repair that does reflect this difference. We have shown that, while juvenile (weaned) pigs recover rapidly after ischemic intestinal injury, barrier repair is markedly underdeveloped in neonatal (nursing) pigs due to complete failure of epithelial restitution. Importantly, we found that restitution in neonates can be rescued by the direct application of homogenized mucosa from ischemia-injured small intestine from juvenile pigs. The mechanisms that allow for this restitution and rescue remain to be defined. We hypothesized that by identifying a subpopulation of restituting enterocytes by their expression of cell migration transcriptional pathways, we can then predict novel upstream regulators of age-dependent restitution response programs. Superficial mucosal epithelial cells collected from recovering ischemic jejunum of juvenile pigs were processed for single cell RNA sequencing, unbiased clustering and upstream regulator analysis. A porcine intestinal epithelial cell line (IPEC-J2) and banked tissues from prior rescue experiments were qualitatively and functionally assessed for activity of predicted upstream regulators. Single cell transcriptomics in recovering juvenile epithelium revealed a subcluster of absorptive enterocytes that express several cell migration pathways key to restitution. Differentially expressed genes in this subcluster predicted their upstream regulation by many potential molecules, including colony stimulating factor-1 (CSF-1) which is known to induce cell migration in non-intestinal epithelial tissues. To begin validating this prediction, we demonstrated that CSF-1 was enriched in the ischemic juvenile mucosa which rescues neonatal restitution and documented expression of the CSF-1 receptor (CSF1R) in both neonatal and juvenile epithelium, indicating that these cells are equipped to respond to CSF-1. CSF-1 and CSF1R co-localized in ischemic juvenile, but not neonatal, wound-adjacent epithelial cells and in the restituted epithelium of juveniles and rescued (but not control) neonates. Further, the CSF1R inhibitor BLZ945 reduced restitution in scratch wounded IPEC-J2 cells. Single cell transcriptomics have the power to inform potential novel therapeutic targets, such as CSF-1, to improve mucosal recovery in neonates with intestinal failure in this unique and powerful pig model. NIH K01 OD028207, NIH R01 HD095876, NIH U01 TR002953, NIH T32 OD011130, NIH P30 DK034987, USDA NIFA 1007263 and 07985. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

  PublisherDOI

• Neonatal colon exhibits enhanced post-ischemic repair relative to the neonatal jejunum

  Physiology · 2023-05-01

  article1st authorCorresponding

  Intestinal ischemia is the most common cause of gastrointestinal-related morbidity and mortality within the neonatal intensive care unit. Ischemia-induced loss of the intestinal epithelial barrier predisposes patients to life-threatening sepsis unless that barrier is rapidly restored. Early barrier restoration relies on epithelial restitution to achieve wound closure, followed by rearrangement of tight junction proteins to re-establish barrier resistance. To inform putative therapeutics that promote rapid barrier repair in neonates, we have developed a highly-translational model of intestinal ischemia in the neonatal pig. Previous studies have demonstrated a significant defect in post-ischemic repair of the neonatal pig (2-weeks-old) jejunum relative to the juvenile (6-weeks-old) pig. Therefore, we hypothesized that the neonatal colon will demonstrate a similar defect in epithelial barrier repair. Segments of distal jejunum and spiral colon were subjected to surgically-induced ischemia followed by ex vivo recovery on Ussing chambers. Barrier repair was calculated by percent mucosal epithelialization, a measure of restitution, as well as transepithelial electrical resistance, a measure of barrier resistance. Unexpectedly, the ischemically-injured, ex vivo-recovered neonatal colon demonstrated significantly increased epithelial wound healing by restitution (p&lt;0.005) as well as barrier resistance (p&lt;0.05) relative to the neonatal jejunum. Furthermore, scanning electron microscopy revealed that colonocytes demonstrate a restitution phenotype defined by loss of their columnar morphology, marked flattening of their cellular profile and frequent formation of lamellipodia-like processes. Under identical experimental conditions, enterocytes do not demonstrate this phenotypic change. These findings suggest the presence of a colon-specific mechanism of intestinal epithelial barrier repair that is not present in the jejunum. Ongoing experiments aim to better elucidate the inter- and intracellular pathways that define this colon-specific mechanism of repair. Defining these pathways may inform the formulation of future pharmaceuticals that directly upregulate these pathways along the entire length of the intestine and therefore mitigate the effects of ischemic injury in neonates. NIH K01 OD 028207, NIH-NICHD R01 HD095876, U01 TR002953, T32OD011130 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

  PublisherDOI

• Dietary Oligosaccharides Differentially Modulate Microbiome, Enteric Glia, and Epithelial Barrier Function in the Neonatal Jejunum and Colon

  The FASEB Journal · 2022-05-01

  article

  In our pig intestinal ischemia model, a neonatal defect in epithelial barrier restitution in the jejunum can be rescued by ischemic mucosal homogenate from weaned pigs. This is associated with an immature enteric glial cell (EGC) network, a known driver of restitution that matures postnatally partly in response to microbial colonization, which can be modulated with dietary prebiotic fiber. Therefore, we hypothesized that dietary oligosaccharide supplementation accelerates postnatal microbial colonization and EGC network maturation in the jejunum and colon, thus enhancing restitution after ischemic injury. After 24‐hours of colostrum, piglets were fed control or oligosaccharide‐supplemented formula (control‐fed or prebiotic‐fed) for 21 days and fecal swabs were sequenced for 16S rDNA. Intestinal samples were collected for western blot, imaging, and EGC culture. Surgically ischemia‐injured jejunal and colonic mucosal samples from select day 14 pigs were recovered ex vivo while monitoring epithelial barrier function by transepithelial electrical resistance (TEER). Migration abilities, calcium responses to ATP, paracrine effects on IPEC‐J2 cell restitution, and protein secretome were assessed in jejunal and colonic EGC cultures. Colonic microbial taxa changed in a time‐ and diet‐dependent manner with the prebiotic‐fed taxa clustering by day 7 and becoming progressively more tightly clustered over time (P&lt;.050). TEER and histology of uninjured jejunum and colon were unaffected by diet. Following ischemia, low initial TEER recovered to control levels in the control‐fed colon but not prebiotic‐fed colon (diet and injury interaction, P=.038), while diet had no effect on jejunal TEER recovery. Prebiotic‐fed colon had lower levels of the EGC markers glial fibrillary acidic protein (GFAP) and S‐100B at day 21 (P&lt;.050), and subjectively reduced density of GFAP + and S‐100B + EGC were noted in preliminary volume imaging of prebiotic‐fed jejunal submucosa at days 14 and 21. EGC from prebiotic‐fed colonic submucosa showed decreased chemotactic motility toward sterile‐filtered colonic contents (P=.010), decreased intracellular calcium response to ATP (P=.0075), and their co‐culture with IPEC‐J2 enhanced epithelial restitution versus monoculture (P=.032). Oppositely, EGC from prebiotic‐fed jejunal submucosa showed increased intracellular calcium response (P=.050) and their co‐culture with IPEC‐J2 did not enhance restitution as efficiently (P=.33) as those from control‐fed jejunal submucosa (P=.019). For future study, prebiotic‐fed colonic submucosal EGC differentially secreted 13 proteins of interest versus control‐fed. Preliminary results indicate dietary oligosaccharides in neonates exert different effects in the jejunum versus the colon on EGC network development and phenotype, and on epithelial restitution in vivo and in vitro . Ongoing work to understand microbiome‐ EGC‐epithelial interactions during postnatal development may lead to novel preventative and clinical practices to improve intestinal health in vulnerable neonates.

  PublisherDOI

• Porcine Models of the Intestinal Microbiota: The Translational Key to Understanding How Gut Commensals Contribute to Gastrointestinal Disease

  Frontiers in Veterinary Science · 2022 · 49 citations

  1st authorCorresponding
  • Medicine
  • Biology
  • Immunology

  In the United States, gastrointestinal disorders account for in excess of $130 billion in healthcare expenditures and 22 million hospitalizations annually. Many of these disorders, including necrotizing enterocolitis of infants, obesity, diarrhea, and inflammatory bowel disease, are associated with disturbances in the gastrointestinal microbial composition and metabolic activity. To further elucidate the pathogenesis of these disease syndromes as well as uncover novel therapies and preventative measures, gastrointestinal researchers should consider the pig as a powerful, translational model of the gastrointestinal microbiota. This is because pigs and humans share striking similarities in their intestinal microbiota as well as gastrointestinal anatomy and physiology. The introduction of gnotobiotic pigs, particularly human-microbial associated pigs, has already amplified our understanding of many gastrointestinal diseases that have detrimental effects on human health worldwide. Continued utilization of these models will undoubtedly inform translational advancements in future gastrointestinal research and potential therapeutics.

  PublisherOA PDFDOI

Frequent coauthors

• Amanda L. Ziegler

  North Carolina State University

  7 shared

• Anthony T. Blikslager

  North Carolina State University

  5 shared

• Lisa A. Edwards

  Veterinary Medical Teaching Hospital

  4 shared

• Daniela Orellana-Guerrero

  Veterinary Medical Teaching Hospital

  4 shared

• Susanne Pfeiffer

  Hong Kong Jockey Club

  4 shared

• Julia A. Beatty

  City University of Hong Kong

  4 shared

• Andrew W. Oates

  Colorado State University

  4 shared

• Catherine D. Renaudin

  Veterinary Medical Teaching Hospital

  4 shared

Labs

• Anatomic Pathology LaboratoryPI

Education

• PhD, Comparative Biomedical Sciences

  NC State University College of Veterinary Medicine

  2023

• DVM

  University of Georgia

  2017

• B.S. Biochemistry

  University of Virginia

  2012

Awards & honors

• T32 Fellowship, National Institutes of Health, 2022
• COHA Translational Research Fellowship, CTSA One Health Alli…
• C.L. Davis Award, Davis-Thompson Foundation, 2019
• American College of Veterinary Pathologists Award for Excell…
• Distinguished Majors Program-Highest Honors, The University…