About

Sarah Ho is the CVM Director of Student Engagement at the College of Veterinary Medicine at NC State University. Her role involves fostering student involvement and supporting their academic and personal growth within the college community. The page highlights her contact information and her position as a key figure in student engagement, but does not provide specific details about her research focus, background, or key contributions in the field of veterinary medicine or biomedical sciences.

Research topics

• Genetics
• Biology
• Chemistry
• Medicine
• Organic chemistry
• Cell biology
• Chemical engineering
• Cancer research
• Internal medicine
• Inorganic chemistry

Selected publications

• Myeloid cell-specific HMGB1 deficiency exaggerates mucoinflammatory responses but promotes bacterial clearance in mucoinflammatory lung disease

  Scientific Reports · 2026-01-12

  articleOpen accessSenior authorCorresponding

  High mobility group box 1 (HMGB1), a highly conserved nuclear protein, is released into the extracellular milieu serving as a modulator of inflammatory responses. HMGB1 levels are elevated in the airspaces of CF patients and mice with cystic fibrosis (CF)--like lung disease. To reduce extracellular release of HMGB1 into the lung airspaces, we previously introduced airway epithelial cell-specific HMGB1 deficiency in Scnn1b-Tg+ (Tg+) mice, a model of human CF-like lung disease. While the deletion of airway epithelial cell-specific HMGB1 did not reduce bronchoalveolar lavage fluid (BALF) HMGB1 levels, the intracellular HMGB1 deficiency resulted in exaggerated inflammatory responses. In this study, because HMGB1 protein levels were found significantly elevated in Tg+ BALF cells, we hypothesized that myeloid cell-derived HMGB1 deficiency will reduce extracellular HMGB1 levels in the lung airspaces of Tg+ mice, which will modulate pathological features of lung disease in Tg+ mice. Accordingly, we introduced myeloid cell-specific HMGB1 deficiency in Tg+ mice. The deletion of HMGB1 in myeloid cells did not result in any obvious alterations in the lungs of WT mice. The BALF levels of HMGB1 were comparable between myeloid cell-specific HMGB1-deficient Tg+ and HMGB1-sufficient Tg+ mice. As expected, as compared with the HMGB1-sufficient WT, HMGB1-sufficient Tg+ mice displayed increased total cell counts consisting of neutrophils, eosinophils, and lymphocytes. As compared with the HMGB1-sufficient Tg+ mice, the myeloid cell-specific HMGB1-deficient Tg+ mice exhibited significantly increased BALF neutrophil and eosinophil counts, which was associated with increased BALF levels of granulocyte-specific chemoattractants, i.e., KC/CXCL1, MCP-1/CCL2, MIP-1α/CCL3, and MIP-1β/CCL4, Th2 lymphocyte-specific chemoattractants, i.e., TARC/CCL17 and MDC/CCL22, and monocyte-specific chemoattractants, i.e., MCP-3/CCL7 and MCP-5/CCL12. As compared with the HMGB1-sufficient Tg+ mice, the alveolar macrophages from HMGB1-deficient Tg+ mice were significantly enlarged, suggesting their higher activation status. Myeloid cell-specific HMGB1 deletion also resulted in significantly improved clearance of spontaneous bacterial infection in Tg+ mice. Furthermore, myeloid cell-specific HMGB1 deletion significantly worsened pathological manifestations in Tg+ mice, i.e., exaggerated airway mucus obstruction, increased peribronchiolar infiltration of inflammatory cells, increased alveolar space enlargement, and increased lymphoid hyperplasia. Collectively, although myeloid cells are not the source of extracellular HMGB1 found in the inflamed airspaces of Tg+ mice, the myeloid cell-specific HMGB1 deficiency modulates key pathological features of mucoinflammatory lung disease in these mice.

  PublisherOA PDFDOI

• Deficiency of ZFP36L1 and ZFP36L2 impairs liver homeostasis and initiates cholestatic liver injury

  Hepatology Communications · 2026-04-17

  articleOpen accessSenior authorCorresponding

  BACKGROUND: RNA-binding proteins, Zinc Finger Protein 36-Like 1 (ZFP36L1) and Zinc Finger Protein 36-Like 2 (ZFP36L2), post-transcriptionally regulate the expression of a large number of genes involved in various cellular processes. However, specific or redundant functions of ZFP36L1 and ZFP36L2 in liver homeostasis have never been explored. Here, we hypothesized that ZFP36L1 and ZFP36L2 are functionally redundant in the liver, and their combined deficiency would stabilize their direct mRNA targets, which would alter liver homeostasis. METHODS: We generated combined liver-specific ZFP36L1-deficient and ZFP36L2-deficient mice (L1/L2dKO) and compared their liver homeostatic parameters with flox control (L1/L2FLX) mice. We performed detailed analyses of liver histology, serum biomarkers of liver injury, liver transcriptome, bile flow rate, and biliary total bile acid (TBA) excretion. RESULTS: We demonstrated that the combined liver-specific deficiency of ZFP36L1 and ZFP36L2 in mice (L1/L2dKO) results in spontaneous cholestatic liver injury, which was characterized by elevated hepatic and serum levels of TBAs and liver injury biomarkers, including ALP, ALT, and AST, presence of bile infarcts followed by marked inflammation, cellular proliferation, and fibrosis. To determine the impact of deficiency of ZFP36L1 and ZFP36L2 on the liver transcriptome and their relevance to cholestatic liver injury, RNA sequencing of whole livers of L1/L2dKO and L1/L2FLX mice was performed, which showed significant perturbation of ZFP36L1/ZFP36L2 target genes associated with cholestasis in L1/L2dKO mice. In addition, L1/L2dKO mice exhibited reduced bile flow rate and decreased biliary TBA excretion. Subsequent analyses revealed impaired bile canalicular morphogenesis by postnatal day 7, as evidenced by F-actin and zonula occludens-1 staining patterns. CONCLUSIONS: Our findings demonstrate beneficial roles of ZFP36L1 and ZFP36L2 in maintaining liver homeostasis.

  PublisherDOI

• Impacts of Mislabeled ECIG Liquids on Primary Particulate Matter Emissions

  Toxics · 2026-03-13

  articleOpen access

  Electronic cigarette (ECIG) liquids are marketed with labeled nicotine concentrations and propylene glycol (PG) to vegetable glycerin (VG) ratios, yet quality control inconsistencies may alter vaping emissions. We quantified discrepancies between labeled and measured chemical content and evaluated how these differences affect emissions of particulate matter with an aerodynamic diameter of 2.5 µm or smaller (PM2.5). Flavor-free liquids (n = 20) spanning nicotine labels of 0, 9, 18, and 48 mg/mL and PG content from 0% to 80% were purchased. Nuclear magnetic resonance spectroscopy measured nicotine, PG, and VG. Aerosols were generated using a standardized device in a controlled exposure chamber. PM2.5 was measured using a pDR-1500 and SMPS/APS, with gravimetric correction factors calculated. Labeling inaccuracies were widespread: “nicotine-free” liquids contained 0.1 to 0.4 mg/mL nicotine, and labeled nicotine deviated by up to ±30%. PG/VG ratios were frequently incorrect; 70% of samples contained higher VG than labeled, including “100% VG” products with about 10% PG. Higher VG consistently increased PM2.5 mass, while nicotine had a minimal effect. The pDR overestimated mass, whereas SMPS/APS underestimated due to volatilization losses. Overall, inaccurate ECIG liquid labeling can alter measured PM2.5 emissions under controlled conditions.

  PublisherOA PDFDOI

• Single-cell transcriptomics reveal alveolar macrophage-specific responses in single-hit ozone exposure model in mice

  American Journal of Physiology-Lung Cellular and Molecular Physiology · 2026-01-02

  articleOpen accessSenior author

  This study addresses a critical knowledge gap regarding the response of alveolar macrophages to ozone, a potent inhaled toxicant. Specifically, we demonstrate that a single exposure to two experimentally relevant concentrations of ozone significantly alters functionally relevant gene expression in alveolar macrophages, as revealed by single-cell resolution analysis.

  PublisherDOI

• Optimizing Neutrophil Recruitment to Tackle Bacterial Infections

  American Journal of Respiratory Cell and Molecular Biology · 2025-01-21 · 1 citations

  letterOpen accessSenior author
  PublisherDOI

• Prior acute ozone injury dampens Th2 responses to subsequent repetitive ozone exposures in mice

  Research Square · 2025-12-09

  preprintOpen accessSenior author
  PublisherOA PDFDOI

• The Innate Lymphoid System Is a Critical Player in the Manifestation of Mucoinflammatory Airway Disease in Mice

  UNC Libraries · 2025-07-31

  articleOpen access

  Innate lymphoid and adaptive immune cells are known to regulate epithelial responses, including mucous cell metaplasia (MCM), but their roles in mucoinflammatory airway diseases, such as cystic fibrosis, remain unknown. <em>Scnn1b</em> transgenic (<em>Scnn1b</em>-Tg⁺) mice, which recapitulate cystic fibrosis-like mucoinflammatory airway disease, deficient in innate lymphoid (<em>Il2rg</em> knockout mice [<em>Il2rg</em> ^KO]), adaptive immune (<em>Rag1</em> knockout mice [<em>Rag1</em> ^KO]), or both systems (<em>Il2rg</em> ^KO/<em>Rag1</em> ^KO), were employed to investigate their respective contributions in the pathogenesis of mucoinflammatory airway disease. As previously reported, immunocompetent Tg⁺ juveniles exhibited spontaneous neonatal bacterial infections with robust mucoinflammatory features, including elevated expression of <em>Th2</em>-associated markers accompanied by MCM, elevated MUC5B expression, and airway mucus obstruction. The bacterial burden was increased in <em>Il2rg</em> ^KO/Tg⁺ juveniles but returned to significantly lower levels in <em>Il2rg</em> ^KO/<em>Rag1</em> ^KO/Tg⁺ juveniles. Mechanistically, this improvement reflected reduced production of adaptive immunity-derived IL-10 and, in turn, increased activation of macrophages. Although all the mucoinflammatory features were comparable between the immunocompetent Tg⁺ and <em>Rag1</em> ^KO/Tg⁺ juveniles, the <em>Il2rg</em> ^KO/Tg⁺ and <em>Il2rg</em> ^KO/<em>Rag1</em> ^KO/Tg⁺ juveniles exhibited suppressed expression levels of <em>Th2</em> markers, diminished MCM, suppressed MUC5B expression, and reduced mucus obstruction. Collectively, these data indicate that, in the context of airway mucus obstruction, the adaptive immune system suppresses antibacterial macrophage activation, whereas the innate lymphoid system contributes to MCM, mucin production, and mucus obstruction.

  PublisherDOI

• Repetitive ozone exposure worsens features of muco-inflammatory disease in developed Scnn1b-Tg+ mice lungs

  Frontiers in Toxicology · 2025-05-27 · 2 citations

  articleOpen accessSenior authorCorresponding

  Introduction Ambient exposure to ozone (O 3 ), one of the six criteria pollutants, is associated with the exacerbation of respiratory symptoms in individuals with underlying lung diseases. Using Scnn1b -Tg+ (Tg+) mice, a widely used model of muco-inflammatory lung disease, we have demonstrated that O 3 exposure during the early stages of postnatal lung development leads to exacerbated muco-inflammatory outcomes. However, it remains unclear whether O 3 affects the developed lungs differently than the underdeveloped lungs of Tg+ mice. Methods We exposed 3-week-old wild-type (WT) and Tg+ mice to either filtered air (FA) or 0.8 ppm O 3 for 3 weeks and examined the lung phenotypes 12-16 h post-last exposure. Results As compared to FA-exposed WT mice, O 3 -exposed WT mice showed increased bronchoalveolar lavage fluid (BALF) proteins, increased immune cells, increased inflammation, alveolar space enlargement, and tissue consolidation. As compared to FA-exposed WT mice, the FA-exposed Tg+ mice showed increased immune cells, elevated levels of inflammatory mediators, e.g., IL-5, G-CSF, MIP-2, KC, MIP-1α, MIP-1β, IP-10, TNF-α, and IL-17, increased inflammation, alveolar space enlargement, tissue consolidation. As compared to FA-exposed Scnn1b -Tg+ mice, O 3 -exposed Tg+ mice had increased total protein, total dsDNA, and phagocytosed lipid contents, in addition to exaggerated granulocytic recruitment, peripheral and bronchiolar inflammation, alveolar space enlargement, and tissue consolidation. Discussion Together, our data using Tg+ mice with developed lungs exhibited several findings consistent with previous findings observed in Tg+ neonates. Interestingly, however, as opposed to the previous report in O 3 -exposed neonatal Tg+ mice, where the hallmark features of Tg+ airway disease, i.e., mucus obstruction and expression of major gel-forming mucins (MUC5B and MUC5AC) were found exacerbated by O 3 exposure, the FA- and O 3 -exposed Tg+ mice with developed lungs exhibited comparable responses. These differential responses suggest that the stage of lung development is an important factor in the modulation of epithelial remodeling following O 3 exposure.

  PublisherOA PDFDOI

• Gastroprotective effect of ethanol extract of Ficus virens Aiton bark in ethanol induced in vivo ulcer model and exploring mechanism via molecular docking studies

  Nutrire · 2025-06-02 · 1 citations

  article1st authorCorresponding
  PublisherDOI

• Tristetraprolin protects against ozone-induced acute lung injury and inflammation in mice

  The Journal of Immunology · 2025-12-11

  articleOpen accessSenior author

  Tristetraprolin (TTP) is an anti-inflammatory protein that mediates messenger RNA (mRNA) decay of certain transcripts, especially those encoding proinflammatory cytokines. TTP modulates various pathological outcomes in diverse inflammatory diseases; however, its role in ozone (O3)-induced acute lung injury (ALI) has never been tested. Here, we hypothesized that the loss of TTP would exacerbate O3-induced ALI and that the systemic overexpression of TTP would mitigate O3-induced ALI. Accordingly, TTP-knockout (TTPKO), airway epithelial cell-specific TTP-deficient (EpiKO), myeloid cell-specific TTP-deficient (MyeKO), and systemic TTP-overexpressing (TTPΔARE) adult male and female mice, along with their respective littermate control TTP-sufficient mice, were exposed to either O3 (3 ppm) or filtered air for 3 h. The endpoints, including bronchoalveolar lavage fluid cellularity, cytokine levels, and histopathological changes, were assessed 21 to 24 h after O3 or filtered air exposure. As compared with the O3-exposed TTP-sufficient mice, the O3-exposed TTPKO and O3-exposed cell-specific TTP-deficient mice exhibited a significant worsening of ALI outcomes (i.e., neutrophil infiltration, cytokine/chemokine production, and lung pathology). The severity of these outcomes was comparatively milder in O3-exposed EpiKO and O3-exposed MyeKO mice than in O3-exposed TTPKO mice. Conversely, the O3-exposed TTPΔARE mice were protected against O3-induced ALI, as indicated by relatively reduced levels of inflammatory cytokines/chemokines, reduced neutrophil infiltration, and mitigated lung pathology. Collectively, our data suggest that TTP is a critical regulator of inflammation in O3-induced ALI. These findings indicate that enhancing TTP expression could be a potential therapeutic strategy for simultaneously targeting multiple inflammatory cytokines in O3-induced ALI and possibly other inflammatory diseases.

  PublisherOA PDFDOI

Recent grants

• Center for Lung Biology and Disease

  NIH · $31.1M · 2019–2029

• Understanding the role of myeloid cells in ozone-induced airway disease

  NIH · $2.7M · 2024–2026

Frequent coauthors

• Sonika Patial

  National Institute of Environmental Health Sciences

  43 shared

• Richard C. Boucher

  University of North Carolina at Chapel Hill

  25 shared

• John J. LaPres

  Michigan State University

  20 shared

• Ishita Choudhary

  North Carolina State University

  18 shared

• Wanda K. O’Neal

  University of North Carolina at Chapel Hill

  18 shared

• Thao Vo

  16 shared

• Alessandra Livraghi-Butrico

  16 shared

• Hong Dang

  Lung Institute

  14 shared

Education

• Ph.D., Animal Science

  University of California, Davis

  2006

• M.S., Animal Science

  University of California, Davis

  2002

• B.S., Animal Science

  University of California, Davis

  2000

Awards & honors

• 2022 Dean’s Teacher Merit Honor Award (Class of 2025)
• 2021 Distinguished Research Scholar Award
• 2021 Dean’s Teacher Merit Honor Award (Class of 2024)
• 2020 Dean’s Teacher Merit Honor Award (Class of 2023)
• 2019 LSU Alumni Association Rising Faculty Research Award